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Individuals with diabetes have an increased risk of breast, colorectal, pancreatic and prostate cancer. Metformin, an oral biguanide used to treat diabetes, has anti-hyperglycaemic, anti-hyperinsulinemic and antioxidant activities. The effects of metformin on testicular tissue damage in cancer and diabetic + cancer rat models were evaluated histologically, immunohistochemically and biochemically. The diabetic model was produced in Copenhagen rats using a single dose of streptozotocin (65 mg/kg), while prostate cancer was induced through subcutaneous inoculation of 2 x 10(4) Mat-LyLu cells into the animals. At the end of the experimental period, testicular tissues with a close functional relationship to the prostate were collected. Histological evaluation found moderate to severe damage to testes following the diabetes and cancer process. Histopathological and biochemical impairments were observed in the early stage of prostate cancer, which were increased in the diabetic animals. Metformin administration reversed these injuries and provided substantial protection of the testes. In particular, metformin had protective effects on tissue damage, apoptosis, oxidative stress and antioxidant capacity. This suggests that metformin should be further investigated as a targeted protective drug against prostate cancer-related damage to the testes. Istanbul University

Valproic acid (VPA) is a drug used for the treatment of epilepsy worldwide. Depending on usage, it can cause complications such as coagulopathies, hepatotoxicity, and encephalopathy.

In this present study, the duration of melatonin (Mel) administered to diabetic rats was prolonged so as to examine its effects on the biochemical liver parameters of diabetic rats. In the experiment, Male Sprague Dawley rats were divided randomly into five groups; the control, diabetic + Mel, diabetic, diabetic + insulin, and diabetic + Mel + insulin. Diabetes mellitus was induced by administration of a single dose of streptozotocin (60 mg/kg) intraperitoneally and rats were given vehicle as a solvent for Mel every day for 12 weeks. In the diabetic + Mel group, diabetic rats were administered Mel (10 mg/kg/day) for 12 weeks to treat diabetes. The diabetic + insulin group were diabetic rats given insulin (6 U/kg) subcutaneously for 12 weeks. The diabetic + Mel + insulin rats received insulin and Mel at the same dose and time. At the end of the experiment, the animals were decapitated and liver tissues were taken. The protective effect of Mel on liver tissue of diabetic rats was investigated, total antioxidant status, total oxidant status, reactive oxygen species, oxidative stress index, adenosine deaminase, xanthine oxidase, paraoxonase 1, sodium/potassium ATPase, myeloperoxidase, γ-glutamyl transferase, sorbitol dehydrogenase, tumor necrosis factor-alpha, homocysteine, nitric oxide, glucose-6-phosphate dehydrogenase, and glycoprotein levels were determined in liver tissues. Treatment with Mel and/or insulin has been found to have a protective effect on biochemical parameters. The results showed that administration of Mel to diabetic rats prevented the distortion of the studied biochemical parameters of liver tissues.

The aim of current work was able to show the oxidant effect of cancer cells found in any part of the body on the liver and to investigate the possible protective effect of deuterium-depleted water (DDW) on this oxidant effect by determining of some liver parameters. Ehrlich ascites tumor bearing BALB/c mice were used for this purpose. BALB/c mice were selected randomly and divided into four groups (n = 5 in each group) as control group, tumor group, control+DDW group, tumor+DDW group, fifteen days after tumor cell injection, liver tissue samples were taken for all groups. In the tumor group, liver lipid peroxidation, sialic acid and protein carbonyl levels, xanthine oxidase, myeloperoxidase, catalase, gamma-glutamyl transferase, sorbitol dehydrogenase, glutathione peroxidase and glutathione reductase activities, were significantly higher than those in the control group while glutathione levels and paraoxonase1, sodium potassium ATPase, glutathione-S-transferase, alanine transaminase and aspartate transaminase activities decreased significantly. Compared with the tumor group, the changes in all parameters except sialic acid, catalase, alanine transaminase and aspartate transaminase were reversed in the DDW given tumor groups, while sialic acid and catalase values continued to increase, and alanine transaminase and aspartate transaminase values continued to decrease. In conclusion, the consumption of DDW may be beneficial and protective against excessive oxidative stress in cancer complications.

Diabetes and cancer have common physiological and biochemical mechanisms. Metformin is the preferred drug of choice for the treatment of diabetes. Prostate cancer can be modeled in by injection of MAT-Lylu cells. A model of diabetes in rats is induced by streptozotocin injectıon. In the current study, we explored the mechanisms by which diabetes accelerates cancer, and evaluated the effects of metformin to know whether it has any impact against the damage caused by cancer and diabetic + cancer via histopathological and biochemical parameters of kidney tissue.The experiment was carried out in rats. Groups 1-Control, 2- Diabetic, 3-Cancer, 4-Diabetic + cancer, 5-Diabetic + cancer + metformin, 6-Cancer + metformin. Metformin treatment was applied by gavage every day. The research ended on the 14th day. The collected kidney tissue sections were stained with Hematoxylin-Eosin.Histological evaluation showed moderate to severe damage to the kidney tissue following diabetic and cancer processess. In diabetic, cancer and diabetic + cancer groups, reduced glutathione levels, total antioxidant status, sodium/potassium-ATPase and paraoxonase1 activities were found to be significantly abated. While advanced oxidized protein products, lipid peroxidation, nitric oxide, tumor necrosis factor-alpha, reactive oxygen species levels, total oxidant status, catalase, superoxide dismutase, glutathione-related antioxidant enzymes, myeloperoxidase, and arginase activities were significantly raised. The administration of metformin reversed these defects. The outcome of the reveals that histopathological and biochemical damage in cancer and diabetes + cancer groups decreased in the groups that received metformin.In conclusion, metformin treatment can be considered an adjuvant candidate for kidney tissue in diabetes, prostate cancer and cancer therapy related damage.

In this study, the effect of metformin on boron levels and oxidative brain damage in rats due to diabetes and prostate cancer was investigated for the first time. Myeloperoxidase (MPO) activity and the amount of DNA were investigated as tissue oxidative and toxic damage parameters. In Copenhagen rats, Dunning prostate cancer was induced using high metastatic MAT-Lylu cells and diabetes was induced by single dose of streptozotocin (STZ) injection. Metformin was administered for 14 days after diabetes and prostate cancer induced. The rats were divided into six groups as follows: control group, diabetic group (D), cancer group (C), diabetic + cancer (DC) group, cancer + metformin (CM) group, diabetic + cancer + metformin (DCM) group. At the end of the experiment, brains were removed. Significant decrease of brain boron levels and significant elevation of MPO activity and DNA levels were observed in D, C, and DC groups as compared to control group. The effect of diabetes induction on the brain boron levels was much more than prostate cancer induction. The administration of metformin with CM and DCM obviously declined MPO activity and increased brain boron levels almost near to control group level. In conclusion, this study shows that the protective effect of metformin against brain damage in STZ-induced diabetic rats with Dunning prostate cancer may also be related to increased boron levels. The boron levels may be a novel indicator of reduced toxic and oxidative stress. Furthermore, the distribution and mechanism of action of boron should be clarified.

The current study was designed to investigate the effects of zinc sulfate on cell proliferation, metallothionein (MT) immunoreactivity and antioxidant system against acute ethanol-induced oxidative damage in tongue tissues of rats. Wistar albino male rats, 2.5 to 3.0 months, were divided into four groups: Group I (n = 8), intact control rats; group II (n = 8), control animals given only zinc sulfate (100 mg/kg/day, for 3 consecutive days); group III (n = 14), animals given 1 mL absolute ethanol; group IV (n = 11), animals given zinc sulfate and absolute ethanol at the same dose and time. Animals were sacrificed under anesthesia 2 h after ethanol administration or 4 h after the last zinc sulfate treatment. Ethanol administration caused a marked decrease in the number of MT immunopositive cells and the proliferating cells in the lingual epithelium. A statistically significant decline in reduced glutathione levels, catalase activity and superoxide dismutase activities was also observed, whereas a significant elevation of lipid peroxidation levels and lactate dehydrogenase activities was detected in the ethanol group. In contrast, these changes were reversed by administration of zinc sulfate to ethanol-treated rats. In conclusion, it shows that zinc sulfate has therapeutic effects on acute ethanol-induced oxidative damage in the tongue tissues of rats.

The objective of this study was to examine the protective effects of S-methyl methionine sulfonium chloride (MMSC) against galactosamine (GalN)-induced brain and cerebellum injury in rats. A total of 22 female Sprague-Dawley rats were randomly divided into four groups as follows: Group I (n = 5), intact animals; Group II (n = 6), animals received 50 mg/kg/day of MMSC by gavage technique for 3 consecutive days; Group III (n = 5), animals injected with a single dose of 500 mg/kg of GalN intraperitoneally (ip); and Group IV (n = 6), animals injected with the same dose of GalN 1 h after MMSC treatment. After 6 h of the last GalN treatment (at the end of the experiments), all animals were killed under anesthesia, brain and cerebellum tissues were dissected out. Reduced glutathione, total antioxidant status levels, and antioxidant enzymes (catalase, superoxide dismutase, and glutathione-related enzymes), aryl esterase, and carbonic anhydrase activities remarkably declined whereas advanced oxidized protein products, reactive oxygen species, total oxidant status, oxidative stress index levels, and myeloperoxidase, acetylcholinesterase, lactate dehydrogenase, and xanthine oxidase activities were significantly elevated in the GalN group compared with intact rats. In contrast, the administration of MMSC to GalN groups reversed these alterations. In conclusion, we may suggest that MMSC has protective effects against GalN-induced brain and cerebellar toxicity in rats.

Galactosamine (GalN) is a well-known agent for inducing viral hepatitis models in rodents, but it can cause toxicity on different organs. Vitamin U (Vit U) has been proved as a powerful antioxidant on many toxicity models. The present study was designed to investigate the protective effects of Vit U on GalN-induced stomach injury. Rats were divided into four groups as follows: control (group I), Vit U given animals (50 mg/kg per day; group II), GalN administered animals (500 mg/kg at a single dose; group III), GalN + Vit U given animals (at the same dose and time, group IV). At the end of the 3rd day, animals were killed, and stomach tissues were taken. They were homogenized and centrifuged. In comparison to the control group, glutathione, total antioxidant capacity levels, catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and Na

Pentylenetetrazole (PTZ) is preferred for experimental epilepsy induction. PTZ damages brain and other organs by elevating oxidative substances. Vitamin U (Vit U) is sulfur derivative substance that proved to be an excellent antioxidant. The current study was intended to determine the protective role of Vit U on PTZ-induced brain damage. Male Sprague-Dawley rats were separated into four groups. The Control group (Group I), was given saline for 7 days intraperitoneally (i.p); Vit U (Group II) was given as 50 mg/kg/day for 7 days by gavage; PTZ was injected into animals (Group III) at a single dose of 60 mg/kg, by i.p; PTZ + Vit U group (Group IV) was administered PTZ and Vit U in same dose and time as aforementioned. After the experiment was terminated, brain tissues were taken for the preparation of homogenates. In the PTZ group, glutathione and lipid peroxidation levels, alkaline phosphatase, myeloperoxidase, xanthine oxidase, acetylcholine esterase, antioxidant enzyme activities, total oxidant status, oxidative stress index, reactive oxygen species, and nitric oxide levels were increased. However, total antioxidant capacity was decreased in the PTZ group. Vit U ameliorated these effects in the PTZ-induced brain damage. Consequently, we can suggest that Vit U protected brain tissue via its antioxidant feature against PTZ kindling epilepsy.

The stomach is among the organs grossly affected organ by diabetic complications. The present study was aimed at investigating the protective role of zinc on stomach of streptozotocin (STZ)-induced diabetes mellitus. Female Swiss albino rats were divided in four experimental groups: Group I, control; group II, control + zinc sulfate; group III, STZ-induced diabetic animals; and group IV, STZ-diabetic + zinc sulfate. Diabetes was induced by intraperitoneal injection of STZ, at a dose of 65 mg/kg body weight. Zinc sulfate (100 mg/kg body weight) was given daily by gavage for 60 days to groups II and IV. At the end of the experiment, the rats were sacrificed, and the tissues were taken. In the diabetic group, hexose, hexosamine, fucose, and sialic acid levels, as well as tissue factor, adenosine deaminase, carbonic anhydrase, xanthine oxidase, lactate dehydrogenase, prolidase activities, advanced oxidized protein products, homocysteine, and TNF-α levels were increased in the stomach tissue homogenates. Whereas, catalase, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase, glutathione reductase, paraoxonase, and aryl esterase activities were decreased in the diabetic group. The administration of zinc reversed all the deformities. These findings suggest that zinc has protective role in ameliorating several mechanisms of STZ-induced diabetic stomach injury.

In this study, both diabetes and Dunning prostate cancer were induced for the first time in Copenhagen rats in vivo. Thus, the effects of metformin against heart tissue damage of these rats were investigated by biochemical methods. Dunning prostate cancer was induced in Copenhagen rats using high metastatic MAT-LyLu cells. The rats were divided as follows: Control group: only injected with 0.9% NaCl for 14 days; Diabetic group: only injected single dose of streptozotocin (STZ) (65 mg/kg); Cancer group: subcutaneously (s.c) inoculated with 2 x 104 MAT-LyLu cells only; Diabetic + cancer (DC) group: inoculated with 2 x 104 MAT-LyLu cells and STZ injection, Cancer + metformin (CM) group: injected with metformin for 14 days after Mat-LyLu cells application; Diabetic + cancer + metformin (DCM) group: metformin administered for 14 days together with STZ and Mat-LyLu cells. At the end of the experimental period, heart tissues were taken. Reduced glutathione and total antioxidant status levels in heart tissues were decreased, whereas lipid peroxidation, advanced oxidized protein products, nitric oxide, homocysteine, and reactive oxygen species levels, total oxidant status and catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase and xanthine oxidase activities increased in the diabetic, cancer and DC groups. Treatment with metformin reversed these effects. In conclusion, the present study shows that metformin has a protective effect against heart tissue damage in STZ-induced diabetic rats with Dunning prostate cancer.

Vanadium compounds are being investigated as potential therapeutic agents in the treatment of many health problems, primarily diabetes. We aimed to provide the effect of N(1)-4-hydroxysalicylidene-N(4)-salicylidene-S-methyl-isothiosemicarbazidato-oxovanadium(IV) (VOL) on small intestinal injury in experimental male diabetic rats. Four groups were created of 3.0-3.5-month-old rats. The rats were made diabetic by a single dose of streptozotocin (STZ) at 65 mg/kg and grouped as follows: control animals, VOL-given control animals, STZ-induced diabetic animals and STZ-induced diabetic animals given VOL. A daily dose of 0.2 mM/kg vanadium complex was administered orally for 12 days after the inducement of diabetes. On the 12th day, small intestine tissue samples were taken. According to the data obtained from the biochemical analysis, reduced glutathione (GSH) level, catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD), Na+/K+-ATPase and paraoxanase (PON) activities were increased, whereas sialic acid (SA), xanthine oxidase (XO) and disaccharidases (maltase and saccharidase) activities were decreased in the small intestine tissue of VOL-treated diabetic rats. Microscopic examinations revealed a remarkable decrease in the mucosal necrotic areas, discontinuity in the brush border, deterioration of the villi integrity and oedema inside the villi, but with a mild decrease in the inflammatory cells, deterioration and loss of integrity of the gland in the small intestine of VOL-treated diabetic rats. Moreover, VOL treatment markedly decreased the proliferation of villus cells and especially inflammatory cells in the small intestine of diabetic rats. According to the obtained data, the administration of VOL is a potentially convenient strategy to reducing small intestine injury in diabetic rats.

Boron concentrations in 335 tap water samples collected from 75 cities in Turkey have been determined by inductively coupled plasma-mass spectrometry. Boron levels ranged between 0.001 and 5.5 mg/L...

Objective: Amiodarone is used in the treatment of arrhythmia and has been shown to cause side effects in various organs. White cabbage (Brassica oleracea L. var. capitata) is a widely consumed vegetable. The effects of exposure to amiodarone and white cabbage consumption on heart tissue has not previously been investigated. We aimed to investigate the effects of white cabbage extract on amiodarone given to rats’ cardiac tissues. Material and Method: Rats were given white cabbage extract and amiodarone by gavage for seven days. Amiodarone was applied 1 hour after administration of the white cabbage extract. On the eighth day, the hearts of the animals were taken and homogenized. The levels of lipid peroxidation (LPO), reduced glutathione (GSH), sialic acid (SA) and activities of glutathione-S-transferase (GST), catalase, superoxide dismutase (SOD) and tissue factor (TF) were determined. Results: The GSH level, CAT and SOD activities decreased, while the LPO and SA levels increased in the amiodarone treated group. The White cabbage extract prevented any damage of the amiodarone by decreasing the amount of LPO and SA and also strengthened the antioxidant defence system by increasing the amount of the GSH and SOD activities and the CAT and GST activities. Conclusion: It is suggested that the consumption of white cabbage could be an alternative approach to the prevention of the adverse effects of amiodarone on heart tissue. Amaç: Aritmi tedavisinde kullanılan amiodaronun çeşitli organlarda yan etkilere neden olduğu gösterilmiştir. Beyaz lahana (Brassica oleracea L. var. capitata) yaygın olarak tüketilen bir sebzedir. Amiodaron maruziyeti ve beyaz lahana tüketiminin kalp dokusu üzerindeki etkileri araştırılmamıştır. Beyaz lahana ekstraktının amiodaron uygulanan sıçanların kalp dokuları üzerindeki etkilerini araştırmayı amaçladık. Gereç ve Yöntem: Sıçanlara yedi gün boyunca gavajla beyaz lahana ekstresi ve amiodaron verildi. Beyaz lahana ekstresinin uygulanmasından 1 saat sonra amiodaron uygulandı. Sekizinci günde, hayvanların kalpleri alındı ve homojenize edildi. Lipit peroksidasyon (LPO), indirgenmiş glutatyon (GSH), siyalik asit (SA) düzeyleri ile glutatyon-S-transferaz (GST), katalaz, süperoksit dismutaz (SOD) ve doku faktörü (TF) aktiviteleri belirlendi. Bulgular: Amiodaron verilen grupta GSH, CAT, SOD aktiviteleri azalırken LPO ve SA seviyeleri arttı. Beyaz lahana, LPO ve SA miktarını azaltarak amiodaron zararını önledi. Ayrıca GSH düzeyleri ile SOD, CAT ve GST aktivitelerini artırarak antioksidan savunma sistemini güçlendirdi. Sonuç: Beyaz lahana tüketiminin, amiodaronun kalp dokusunda olumsuz etkilerini önlemek için alternatif bir yaklaşım olabileceği ileri sürülebilir.

Moringa oleifera is a source of food, shelter and traditional medicine for many people in developing countries. It is an exceptional source of vitamins, minerals, amino acids, lipids, carotenoids, flavonoids, sterols and phenolics. Owing to its diverse nutritional and phytochemical composition, it is widely consumed and used in therapeutics. In this study, the aqueous, methanol, hexane and ethyl acetate extracts of M. oleifera seeds, leaves and roots were assessed for in vitro α-amylase, α-glucosidase and glucose-induced bovine serum albumin glycation inhibition. Findings indicate that methanol and hexane leaves extracts demonstrated highest α-amylase inhibitory activity (IC50 = 8.217 and 9.397 mg/ml respectively), though the activities were lower than that of acarbose (IC50 = 0.036 mg/ml). In contrast, hexane root extract exhibited optimal α-glucosidase inhibition and antiglycation effect (IC50 = 0.382 and 0.772 mg/ml, respectively). The extract activity was higher than that of acarbose (IC50 = 0.884 mg/ml), but lesser than rutin (IC50 = 0.199 mg/ml); which were the control for α-glucosidase inhibition and antiglycation studies respectively. In conclusion, suggesting its potentials in regulating postprandial blood glucose, and attenuating the production/accumulation of advanced glycation end product. Thus, M. oleifera extracts exhibited promising antidiabetic activity.

Diabetes is usually accompanied by increased production of free radicals or impaired antioxidant defenses. The brain is a target tissue of the oxidative attacks caused by diabetes, and there are observed changes in the biochemical parameters of this tissue in the hyperglycemic state. In this study, we aimed to show the effect of N(1)-2,4-dihydroxybenzylidene-N(4)-2-hydroxybenzylidene-S-methyl-thiosemicarbazidato-oxovanadium (IV) (VOL) compound on diabetic damaged brain tissue, induced by streptozotocin (STZ) on 3.0-3.5-month-old male rats. Single dose of STZ at 65 mg/kg was used to make rats diabetic. Four groups were created randomly. Group (i): control (intact) animals; Group (ii): VOL given control animals; Group (iii): STZ-induced diabetic animals; and Group (iv): orally VOL administered STZ-induced diabetic rats. VOL (0.2 mM/kg/day) administration to control and diabetic animals was performed for a period of 12 days. At the end of day 12, the brain tissues were taken and homogenized. The clear supernatants were used for the determination of glutathione (GSH), lipid peroxidation (LPO), nonenzymatic glycosylation (NEG), and protein levels. Alanine and aspartate transaminases and acetylcholinesterase (AChE), myeloperoxidase (MPO), xanthine oxidase (XO), and oxidative stress marker enzymes activities were also estimated from the homogenates. According to the obtained results, there is found significant elevation of MDA and NEG levels and activities of transaminases, MPO and XO; whereas the GSH content and the activities of AChE and antioxidant enzymes were strongly decreased in the STZ-induced diabetic brain tissues in comparison to control group animals. Twelve days of administration of VOL complex to the diabetic animals reversed all biochemical parameters significantly in diabetic brain tissues. Our findings suggest that the VOL complex may be an ideal candidate to be used as an anti diabetic agent to improve oxidative injury and protect the brain tissue against damage caused by diabetes. This healing effect of the VOL complex may be due to its antioxidant activity and the insulin-mimetic effects of vanadium.

Valproic acid n-dipropyl-acetic acid, VPA) is a medication used as anticonvulsant in the treatment of bipolar disorder, and for migraine prophylaxis. Long-term use of VPA is known to trigger reproductive impairment, which is mediated by elevation of testicular oxidative stress. Edaravone is used in the treatment of cerebrovascular diseases. It can diffuse into many disease-affected organs, thus shows protective effects in numerous tissues including the heart, lung, and testis. The main goal of the present study was to determine the possible protective role of edaravone against VPA-induced oxidative testicular injury. Male Sprague Dawley rats were assigned into four groups. Control rats; rats given only edaravone (30 mg/kg/day); rats given only VPA (500 mg/kg/day); rats given VPA+edaravone for seven days. Edaravone and VPA were applied intraperitoneally. After eight days, testicular tissues were taken from rats. There was a statistically significant increase in the levels of reduced glutathione, lipid peroxidation, reactive oxygen species, total oxidant status, oxidative stress index, and DNA contents as well as catalase, superoxide dismutase, glutathione-related enzymes, gamma-glutamyl transferase, acid and alkaline phosphatases, lactate dehydrogenase, myeloperoxidase and sorbitol dehydrogenase activities in VPA group. More so, advanced oxidized protein products, protein carbonyl, and nitric oxide levels were also significantly increased in VPA group. Activities of glucose-6-phosphate dehydrogenase and sodium/potassium ATPase and total antioxidant status levels remarkably decreased in VPA given group. Treatment with edaravone to VPA group significantly reverted these alterations. These findings demonstrate that administration of edaravone has a beneficial effect against testicular injury in VPA-induced oxidative stress. Istanbul University-Cerrahpasa Scientific Research Projects Unit

Objective: Natural ingredients derived from plants (especially edible ones) continue to be investigated for understanding whether they have therapeutic/preventive effects on certain ailments, such as cancer and gastrointestinal disorders. The main goal of the current work is to investigate the inhibitory potential of Eremurus spectabilis M. Bieb. extracts on histone deacetylase (HDAC), xanthine oxidase (XO) and urease activities. Material and Method: Fresh E. spectabilis leaves were obtained from a local market in Eyup/Istanbul. Inhibitory activities of ethanolic and ethyl acetate extracts on HDAC, XO and urease were examined. Results: According to our findings, ethanolic and ethyl acetate extracts of E. spectabili both have revealed apparent inhibitory effects against all examined enzymes. Ethanolic extract showed a better inhibitory effect on HDAC than ethyl acetate extract. On the other hand, the inhibitory effects of ethyl acetate extract against both XO and urease were higher than the ethanolic extract. Conclusion: Consequently, due to the inhibitory effects of the plant being studied, it might be suggested that it can be used for medicinal purposes, in raw extract form, or as a source of bioactive compounds.

Valproic acid (VPA) is an efficient antiepileptic drug widely used for the treatment of epilepsy and other seizures in both children and adults. It is also reported to have side and toxic effects on many organs and tissues. Vitamin B6 (Vit B6 ) is a well-described water-soluble vitamin, which has an antioxidant effect. In this study, we aimed to investigate the protective effect of Vit B6 on VPA-induced brain injury. Male Sprague-Dawley rats were divided into four groups. Group I, control animals; Group II, Vit B6 (50 mg/kg/day) given rats; Group III, VPA (500 mg/kg/day) given rats; Group IV, VPA and Vit B6 given rats at same dose and time. VPA and Vit B6 were administered intraperitoneally and orally, respectively, for 7 days. At the end of the experiments, the rats were sacrificed and brain tissues were taken. Protein carbonyl and sialic acid levels, xanthine oxidase, adenosine deaminase, acetylcholine esterase, lactate dehydrogenase, myeloperoxidase activities, total oxidant status, and reactive oxygen species levels were found to be increased, while glutathione and total antioxidant capacity levels, catalase, superoxide dismutase, glutathione-S-transferase, paraoxonase, and glutathione reductase activities were found to be decreased in the VPA group. Administration of Vit B6 reversed these defects in the VPA group. These findings indicate that Vit B6 has a protective effect on VPA-induced brain damage.

Diabetes mellitus (DM) is chronic and metabolic disorder, which is mainly attributed by hyperglycemia. Vanadium salts and their oxo-complexes have been shown to possess insulin-mimetic and anti-diabetic activities in animal models and diabetic patients. The main goal of this study was to investigate the protective effect of oxovanadium(IV) complex based on thiosemicarbazone (VOL) [L: (N(1)-2,4-dihydroxybenzylidene-N-(4)-2-hydroxybenzylidene-S-methyl-isothiosemicarbazidato-oxovanadium(IV)] on glycoprotein components levels and oxidative lung injury of streptozotocin (STZ)-induced diabetic rats. Male Swiss albino rats were separated into four groups. Group I (

Galectin-1 is an important mediator that regulates the T-cell-mediated immune response. It has many other biological functions such as cell growth, immunomodulation, and wound healing. The aim of this study was to reveal the role of galectin-1 on liver morphology, cell proliferation, apoptosis, inflammatory and anti-inflammatory mediators, oxidative stress, and antioxidant system in colitis-mediated hepatotoxicity induced by dextran sulfate sodium (DSS). In the present study, adult mice were divided into four groups: The control group intraperitoneally injected with phosphate buffer saline (I), the group which was orally administered with DSS (II), the control group which was injected with galectin-1 (III), and the group which was given DSS and galectin-1 (IV). DSS administration caused degenerative changes and diffuse necrotic damage, an increase in caspase-3 and cyclooxygenase-2 expression, the levels of lipid peroxidation and tumor necrosis factor-alpha, lactate dehydrogenase, and myeloperoxidase activities, and a decrease in cell proliferation, interleukin-10 levels, and antioxidant system parameters in liver tissues. Treatment of DSS group with galectin-1 reversed these effects and prevented liver damage. This study showed that galectin-1 has proliferative, antiapoptotic, anti-inflammatory, and antioxidant effects against DSS-induced liver injury in mice. It is expected considering all results of this study that galectin-1 may be useful as a protective agent against liver toxicity.

3-methoxysalicylidene N-alkyl-thiosemicarbazones (L) (where alkyl is propyl, butyl, pentyl or hexyl) were synthesized. The reaction of the ONS donor ligands with [MoO2(acac)2] in methanol yielded the mixed ligand complexes bearing a solvent molecule as co-ligand, [MoO2(L)MeOH)]. The ligands and complexes were characterized by using analytical and spectroscopic methods. As a representative sample, the dioxomolybdenum(VI) complex of the N4-butyl-substituted thiosemicarbazone was crystallographically examined to ensure the expected structures. X-ray data showed a distorted octahedral environment of molybdenum center. Tyrosinase, collagenase inhibition and antioxidant properties of the compounds were investigated using spectroscopic methods. The ligand and complexes exhibited the different inhibitory activities depending on N-alkyl substituents. Similarly, also the antioxidant capacity of the compounds changed in relation to the substituents.

Background: In current dental treatments, with the aim of a preventive approach,it is argued that removing only the infected layer of dentin is sufficient for cavity preparation. However it is impossible to be sure that the infected layer was completely removed. In addition, the cause of secondary caries and post operative sensitivities has been reported as residual bacteria in some studies. The aim of this study is to investigate the antibacterial and photo-active properties of Cotinus coggygria Scop., Rumex cristatus DC., Beta vulgaris L.var.cicla and Eruca sativa aqueous extracts, and to investigate their usefulness for cavity disinfection in dentistry. Method: The aqueous solutions of plant extracts were prepared to be at a maximum concentration and the Streptococcus mutans solutions mixed with phosphate buffered saline to give 10 8 cfu/mL. A 430–480 nm wavelength light source was used for the irradiation. Three different applications were made: extract + Streptococcus mutans mixture exposed to ligh; extract + Streptococcus mutans mixture that was not exposed to light and S. mutans exposed to light. Results: No antibacterial effect was found for the second and third applications. In the first application, however, irradiation with extract + Streptococcus mutans mixture reduced the number of microorganisms in the beginning by 99% for only Rumex cristatus DC. extract (log 2). Conclusion: Rumex cristatus DC. extract can be used as an alternative in photo-active disinfection of cavities in dentistry. © 2019 Elsevier B.V. SAG-C-DRP-131016-0452 This work was financially supported by the by the Marmara University Scientific Research Projects Commission [grant number SAG-C-DRP-131016-0452 ].

Enzymes are made of protein, that is why they are sensitive molecules and are affected by storage conditions. A small change in enzyme activity during storage may cause a big error in analysis results. The aim of the study was to evaluate the effects of storage time and temperature on urease activity. Urease solutions were prepared at different activities (from 100 to 2000 U/mL) and stored at room temperature, in the refrigerator (4°C), and in the deep freezer (-18°C and -80°C). Activity measurements were made at regular intervals until 28 days by the modified Weatherburn method. The relative activities of 100-1000 U/mL urease solutions stored at room temperature, 4, -18 or -80°C were 75% and below after 4 days. Twenty-eight days later, for 2000 U/mL urease solutions, only at room temperature, the relative activity was reduced to 37%, while at 4, -18 or -80°C, the relative activities were above 80%. Since urease can be maintained at 4°C for 28 days without significant loss of activity, it has practical importance. Low-activity urease solutions (such as 100-1000 U/mL) should not be stored at -18 or -80°C for short or long term storage, they should be stored at 4°C only for one day. Keywords: Urease activity, storage time, storage temperature

This study aimed to investigate the possible neuroprotective effects of bitter melon (BM), chard, and parsley extracts on oxidative damage that may occur in the brain of rats with bile duct ligation (BDL)-induced biliary cirrhosis. It was observed that lipid peroxidation (LPO), sialic acid (SA), and nitric oxide (NO) levels increased; glutathione (GSH) levels, catalase (CAT) activity, and tissue factor (TF) activity decreased significantly in the BDL group. However, in groups with BDL given BM, chard, and parsley extracts LPO, SA, NO levels decreased; GSH levels and CAT activities increased significantly. No significant differences were observed between groups in total protein, glutathione-S-transferase, superoxide dismutase, and boron. Histological findings were supported by the biochemical results. BM, chard, and parsley extracts were effective in the regression of oxidant damage caused by cirrhosis in the brain tissues. PRACTICAL APPLICATIONS: Bitter melon (BM), chard, and parsley have antioxidant properties due to their bioactive compounds which are involved in scavenging free radicals, suppressing their production, and stimulating the production of endogenous antioxidant compounds. Since BM, chard, and parsley extracts were found to be effective in the regression of oxidant damage caused by cirrhosis in the brain tissues, these plant extracts may be an alternative in the development of different treatment approaches against brain damage in cirrhosis. At the same time, these species have been used as food by the people for many years. Therefore, they can be used safely as neuroprotective agents in treatment.

Valproic acid (VPA) is an efficient antiepileptic drug widely used for the treatment of epilepsy and other seizures in both children and adults. It is also reported to have side and toxic effects on many organs and tissues. Vitamin B

The aim of this study was to investigate the cellular mechanisms that cause valproic acid (VPA)-induced liver damage and the therapeutic effect of Vitamin U (Vit U) on these mechanisms. Female Sprague Dawley rats were randomly divided into four groups: intact control animals, animals that received Vit U (50 mg/kg/day), animals given VPA (500 mg/kg/day), and animals given both VPA and Vit U. The rats in the Vit U + VPA group were administered Vit U by gavage an hour before VPA administration every day for 15 days. Liver tissues were evaluated through histopathological, biochemical, immunohistochemical, and Western blotting techniques. Administration of Vit U with VPA resulted in (i) prevention of histopathological changes caused by VPA; (ii) blockage of the decrease in catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities; prevention of the elevation in gamma-glutamyl transferase (GGT) activity and advanced oxidation protein products (AOPP) level; (iii) increased in the levels of interleukin-1 beta (IL-1β), active caspase-3, and cytoplasmic cytochrome c; (iv) increase in cleaved poly (ADP-ribose) polymerase (PARP) level and decrease in LC3B (II/I) ratio; (v) increase in the number of proliferating cells nuclear antigen (PCNA) positive hepatocytes. These findings show that Vit U prevents liver damage caused by VPA through increasing the antioxidant enzyme capacity and hepatocyte proliferation by triggering inflammation and apoptosis. These findings suggest that Vit U provides its protective effects against VPA-induced liver damage by stimulating homeostasis and regeneration.

In this study, we aimed to evaluate whether edaravone (EDA) has a protective role against valproic acid (VPA)-induced lung damage via its antioxidative activity. Male Sprague-Dawley rats were split into four groups. Control (n = 8) rats; rats given EDA (30 mg kg(-1) day(-1); n = 10); rats given only (VPA, 500 mg kg(-1) day(-1); n = 10); rats given VPA + EDA (in the same dose and time) for 7 days. EDA and VPA were applied intraperitoneally. After 8 days, lung tissues were immediately taken from the rats. In lung homogenates, reduced glutathione, total antioxidant status levels, and superoxide dismutase, glutathione peroxidase, sodium/potassium ATPase, paraoxonase1, and carbonic anhydrase activities significantly abated, whereas catalase, glutathione reductase, glutathione-S-transferase activities insignificantly decreased in the VPA-treated group. In contrast, lipid peroxidation, reactive oxygen species, and total oxidant status levels, glycoprotein and protein carbonyl contents, nitric oxide, hydroxyproline levels, and xanthine oxidase, lactate dehydrogenase, arginase, and prolidase activities significantly increased in the VPA-given group. Administration of EDA caused the reverse effects. As a consequence, EDA prevented oxidative stress-mediated lung injury via its robust antioxidant effects.

The present study was aimed at investigating the toxicity of various pesticides on rat liver. It also aimed to show whether this toxicity could be avoided using lupeol. Adult male Wistars albino rats were randomly divided into nine groups. Control groups were given saline, corn oil, and lupeol; pesticide groups were given malathion, chlorpyrifos, and tebuconazole; in the other three treatments, same doses of pesticides and lupeol were given to the rats for ten days. Histopathological examination showed severe degenerative changes in the pesticide groups. Serum AChE activities, liver GSH, total antioxidant capacity levels, AChE, CAT, SOD, GPx, GR, Na

Vitamin U (Vit U) is a novel free-radical scavenger. The protective effect of Vit U on valproic acid (VPA)-induced lung damage was examined. Rats were divided into four groups: control rats; rats given Vit U (50 mg/kg/d, by gavage) for 15 days; rats treated with VPA (500 mg/kg/d, intraperitoneally) for 15 days; and rats were given VPA + Vit U (in same dose and time). On the 16th day of the experiment, the lungs were collected from rats. Lung structure, pulmonary oxidant/antioxidant parameters and Nrf2, α-SMA, and collagen-1 were evaluated by microscopic and biochemical analysis. Additionally, it was determined the interactions of Vit U with Nrf2 and Keap1 by in silico analysis. VPA administration increased lipid peroxidation and the activity of lactate dehydrogenase and myeloperoxidase. However, it decreased the glutathione level, and the activities of glutathione peroxidase, glutathione-S-transferase, catalase, and superoxide dismutase. VPA-mediated oxidative stress prompted structural distortion and fibrotic alterations in the lung. Vit U supplementation reversed structural and biochemical alterations, induced antioxidant system through Nrf2 activation, and attenuated fibrosis by reducing collagen expression in VPA-administered rats. However, Vit U pretreatment was unable to reduce α-SMA levels in the lung of VPA-treated rats. Molecular docking analysis showed the binding of Vit U to ETGE motif leads to dissociation of Nrf2 from the Nrf2/Keap1 complex and its transfer to nuclei. In conclusion, Vit U attenuated VPA-induced tissue damage by restoring antioxidative systems through amelioration of Nrf2 activity in the lung under oxidative stress.

Vanadium compounds are being investigated as potential therapeutic agents in the treatment of many health problems, primarily diabetes. We aimed to provide the effect of N(1)-4-hydroxysalicylidene-N(4)-salicylidene-S-methyl-isothiosemicarbazidato-oxovanadium(IV) (VOL) on small intestinal injury in experimental male diabetic rats. Four groups were created of 3.0-3.5-month-old rats. The rats were made diabetic by a single dose of streptozotocin (STZ) at 65 mg/kg and grouped as follows: control animals, VOL-given control animals, STZ-induced diabetic animals and STZ-induced diabetic animals given VOL. A daily dose of 0.2 mM/kg vanadium complex was administered orally for 12 days after the inducement of diabetes. On the 12th day, small intestine tissue samples were taken. According to the data obtained from the biochemical analysis, reduced glutathione (GSH) level, catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD), Na

Valproic acid (VPA; 2-propyl valeric acid) is a potent drug widely used in treating anxiety disorders, migraine as well as epileptic diseases. In the ongoing study chard protective effect was investigated, on the damaged VPA rat brain. Sprague Dawley rats (females) were grouped as follows: control, VPA (500 mg kg-1 day-1 VPA intraperitoneal), chard (100 mg/kg day chard extract by gavage), VPA + chard (500 mg kg-1 day-1 VPA + 100 mg kg-1 day-1 chard extract). Aqueous chard leaves extract was given 1 hr before apply VPA for a period of 7 days. Lipid peroxidation, advanced oxidation protein products and protein carbonyl content, and superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, and glutathione reductase activities increased in the VPA group. Reduced glutathione levels, paraoxanase, and acetylcholinesterase activities were significantly diminished in the VPA animals. Chard extract application curatively reverted the studied biochemical parameters. The results obtained, it has been found the chard has a protective and antioxidant effect on brain damage induced by VPA. PRACTICAL APPLICATIONS: Valproic acid is a comparably safe pharmaceutical agent, but it can cause severe adverse effects on biological metabolism when it is used in high amount. There are not many studies declared that VPA stimulate the generation of ROS, which is liable for the life-threatening adverse effects of VPA therapy including hepatotoxicity neurotoxicity and teratogenicity. Chard is a plant which has antimicrobial, antibacterial, antiinflammatory, antioxidant, antitumor, antiacetylcholinesterase activities, and hepatoprotective effects. In the current study we examined the protection of the VPA damaged rat brain by chard.

Valproic acid (VPA) is an effective drug, which is preferred for the treatments of epilepsy and various kinds of seizures. Nonetheless, VPA has many life-threatening side effects associated with free radical production. Alpha-lipoic acid (ALA) is a powerful antioxidant, which can scavenge reactive oxygen species (ROS). The effects of ALA against VPA-stimulated brain injury were investigated. In this study, Sprague-Dawley rats were divided as four groups: Group I, control rats; Group II, ALA-administered rats (50 mg/kg/d); Group III, VPA-administered rats (0.5 g/kg/d); Group IV: VPA- and ALA-administered rats at the same dose and time. According to the results, VPA increased lipid peroxidation, protein carbonyl, advanced oxidation protein products, total oxidant status, nitric oxide levels and glutathione-S-transferase, adenosine deaminase, xanthine oxidase activities, decreased glutathione, total antioxidant capacity levels, catalase, superoxide dismutase, glutathione peroxidase, sodium-potassium ATPase, and paraoxonase activities. Treatment with ALA reversed these effects. In conclusion, we may suggest that ALA may be a good candidate for prevention of VPA-induced brain injury.

New thiosemicarbazone-based zinc(II) complexes were synthesized to study their cytotoxicity on A375 malignant melanoma cells. The complexes containing salicylidene (Zn1a), 3-methoxy-salicylidene (Zn1b) or 4-methoxy-salicylidene (Zn1c) moiety were characterized by analytical and spectroscopic methods. Anticancer potential of the complexes was determined by MTT test and HUVEC endothelial cells line was used to comprehend the effect on normal cells. Zn1b with an IC50 of 13 μM was found to be highly cytotoxic against A375 cancer cells, more effective than cisplatin (IC50: 37 μM). Zn1a and Zn1c did not have a negative effect on cell viability in the normal cells and gave the impression that they are more advantageous than cisplatin in this respect. Further, the ability of Zn1a-c to inhibit neuraminidase enzyme and its role in cytotoxicity was discussed. The test revealed that the Zn1b with 3-methoxy substituent exhibited higher inhibition activity against the neuraminidase than the Zn1a and Zn1c as analogical to the cytotoxicity results. In neuraminidase inhibition, IC50 values of Zn1b and Zn1c were 14 and 66 μM, respectively. These concentrations were very close to the cytotoxicity concentrations for Zn1b and Zn1c. The findings may indicate the role of neuraminidase enzyme inhibition in cell death for Zn1b and Zn1c.

Five oxovanadium(IV) complexes were synthesized using acetyl- and benzoylacetone-S-alkyl-thiosemicarbazones (alkyl=methyl, ethyl, propyl or butyl) and salicylaldehyde. Structural characterization was performed by element analysis, infrared, mass and electronic spectra, and also single crystal X-ray crystallography for one sample. The purity of all the complexes was verified with Miller indices (hkl) observed and calculated angles, 2θ values and crystal sizes obtained from powder XRD diffraction. The in vitro cytotoxic activity was determined for the MCF-7, MDA-MB-231 and 3T3 cell lines with an MTT assay for 72 h. The complexes showed cytotoxicity against MCF-7, MDA-MB-231 and 3T3 cells at concentrations of 73–148, 75–224 and 112–176 μM, respectively. All the complexes had better cytotoxicity than the positive control, fluorouracil (5-FU). The complex containing the S-propyl group was the most effective complex, with the concentrations of 72.9 (for MCF-7) and 75.5 (for MDA-MB-231) µM. Furthermore, the ability of the complexes to inhibit elastase, xanthine oxidase and neuraminidase enzymes and their role in cell death was studied. All the complexes inhibited the elastase and xanthine oxidase enzymes at higher concentrations than the IC50 values found for the cytotoxicity. However, the IC50 values for the inhibition of neuraminidase by the complexes bearing ethyl and propyl groups are better than those of quercetin and are close to the values found for the cytotoxicity.

The protective effects of a combination of antioxidants on histopathological changes and biochemical parameters were examined in D-galactosamine (D-GaIN)-induced hepatotoxicity in rats. Physiological saline solution was injected intraperitoneally into the control group, while D-GaIN (500 mg kg-1) was administered intraperitoneally into the experimental animals. The combination of 100 mg/kg/day ascorbic acid, 100 mg/kg/day alpha tocopherol, 15 mg/kg/day beta carotene, and 0.2 mg/kg/day sodium selenate was administered orally to intact control rats for 3 days. The same antioxidant combination was given to the D-GaIN group. Liver and blood samples were used for histopathological and biochemical assays. Liver tissues were significantly damaged by D-GaIN administration based on the histopathological findings. Serum aspartate and alanine transaminase, gamma glutamyl transpeptidase, alkaline phosphatase, lactate dehydrogenase, sialic acid, and uric acid levels increased. Serum and liver glutathione levels decreased, and serum superoxide dismutase, glutathione peroxidase, and glutathione-S-transferase, catalase activities as well as lipid peroxidation values increased in the D-GaIN group. In contrast, administration of the antioxidants reversed the histopathological and biochemical changes in the liver of animals administered D-GaIN. In conclusion, the administration of a combination of antioxidants suppressed histopathological changes and biochemical parameters in rats given D-GaIN.

The aim of this study is to investigate the therapeutic effects of vitamin U (Vit U) on lung tissue of pentyleneterazole (PTZ)-induced seizures in rats. Sprague Dawley male rats were randomly divided into four groups as follows: control (0.9% NaCl given, intraperitoneally); Vit U (50 mg/kg/day, for 7 days by gavage); PTZ; (60 mg/kg one dose, intraperitoneally); and PTZ + Vit U (in same dose and time). At the end of the experiment, lung tissues were taken and examined biochemically and cytologically. Lipid peroxidation (LPO), glutathione (GSH), sialic acid (SA), and nitric oxide (NO) levels, and superoxide dismutase (SOD) and catalase (CAT) activities were determined in lung homogenates. Imprinted lung samples were stained with May Grunwald-Giemsa stain and microscopically examined for the presence of collagen fibers, macrophage, leucocyte, and epithelial cells. PTZ administration significantly increased GSH level and CAT activity and significantly decreased SOD activity compared to the control group. Vit U administration significantly increased GSH level and CAT activity compared to the control group. GSH and NO levels significantly decreased in PTZ + Vit U group compared to the PTZ group. In cytologic analysis, increased collagen fibers, macrophages, leucocytes, and epithelial cells were observed in PTZ group compared to the control group, and Vit U administration decreased these cytological parameters compared to the PTZ group. The findings of this study support the possible protective role of using Vit U as an add-on therapy in order to prevent lung tissue injury which may occur during seizures in epilepsy.

Exposure of biological materials to ionizing irradiation causes accumulation of reactive oxygen species. The current study aimed to investigate whether melatonin or carnosine could provide protection against irradiation-induced small intestinal damage. Forty Wistar albino rats were divided into five groups. Melatonin, carnosine, and combination of carnosine and melatonin were injected into rats in the third, fourth, and fifth groups, respectively. Rats were injected three times every 48 hours. All groups, excluding the control group, were exposed to a dose of 8 Gray whole body gamma irradiation one hour after the second injection. It was determined that irradiation caused degenerative changes in the intestinal tissues, reduced PCNA (proliferating cell nuclear antigen) -positive cell number, and increased caspase-3- and TNF-α (tumour necrosis factor alpha) -positive crypt cell numbers. Results obtained from antioxidant-treated groups were similar to those from the control group. Lipid peroxidation and protein carbonyl levels as well as superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, myeloperoxidase, lactate dehydrogenase and xanthine oxidase activities were increased. However, catalase, sodium potassium ATPase activities and glutathione levels were decreased in the irradiated group of animals. Treatment with antioxidants reversed these changes. It is suggested that exogenous melatonin, carnosine, and melatonin+carnosine combination exhibit protective effects against irradiation-induced small intestinal damage.

Runx2 promotes metastatic ability of cancer cells by directly activating some of the mediators regarding malignancy. Galectin-3 (Gal-3) extensively expressed in normal and transformed cells and it is responsible for many cellular processes. In this study, we aimed to investigate whether there is any relationship between runx2 transcription factor and regulation of galectin-3 expression in different human thyroid carcinoma cell lines. To show effects of runx2 transcription factor on gal-3 expression, we developed runx2 knockdown model in the thyroid carcinoma cell lines; anaplastic 8505C and 8305C and, papillary TPC-1 and follicular FTC-133 by using siRNA transfection. We analyzed the protein expressions and mRNA levels of gal-3 and MMP2/9 in the runx2-silenced cell lines using Western blotting, qPCR, and fluorescent microscopy. Our results showed that mRNA expression levels of gal-3 and MMP2/9 were downregulated in runx2-silenced cell lines. In this investigation, we revealed that regulation of gal-3 expression was strongly correlated with runx2 transcription factor in human thyroid carcinoma. Considering the contribution of human gal-3 in collaboration with MMP2/9 to the malignant characters of many cancers, regulation of their expressions through runx2 seems like one of the key regulatory mechanism for malignant potential of human thyroid carcinoma. Accordingly, runx2 transcription factor inhibitors can be a potential target in order to prevent gal-3 mediated malignancy of human thyroid carcinoma. J. Cell. Biochem. 118: 3911-3919, 2017. © 2017 Wiley Periodicals, Inc.

Objective: Ghrelin is an orexigenic hormone mainly released from the stomachs of rats and takes a significant part in the development of newborn rats. Ghrelin has been shown to possess antioxidant, anti-apoptotic, and anti-inflammatory properties. In this study, we aimed to examine microscopical and biochemical parameters in the kidney of newborn nontreated diabetic and ghrelin-treated diabetic rats. Materials and Methods: Wistar-type newborn rats were divided into four groups. First group: control rats given physiological saline for four weeks; second group: control animals given ghrelin from the third day to the fourth week; third group: diabetic rats given streptozotocin (STZ) on the second day after birth as a single dose; fourth group: diabetic rats given ghrelin from the third day to the fourth week. Results: There was no microscopic difference between the kidney tissues of non-treated diabetic and ghrelin-treated diabetic rats. Lipid peroxidation levels decreased, while superoxide dismutase, catalase activities, and glutathione levels increased in the diabetic group given ghrelin. Serum urea, uric acid, creatinine levels, myeloperoxidase, and xanthine oxidase activities decreased in diabetic rats treated with ghrelin. Conclusion: It can be said that the ghrelin given exogenously has a protective effect in some degree on renal complications in newborn diabetic rats.

Brain damage is a major complication of fulminant hepatic failure. d-Galactosamine (d-GalN)-induced liver toxicity causes damage to brain. The effects of vitamins and selenium mixture against d-GalN stimulated brain injury were investigated in this study. Sprague-Dawley female rats aged 2.0-2.5 months were used for the study. The rats were divided into four categories. A 0.9% NaCl solution was intraperitoneally given to the experimental rats in the first group. Using gavage technique, the second group of animals were subjected to a formulation consisting of 100 mg·kg-1 ·day-1 vitamin C, 15 mg·kg-1 ·day-1 of β-carotene, 100 mg·kg-1 ·day-1 of α-tocopherol in addition to 0.2 mg·kg-1 ·day-1 of sodium selenate for 3 days. The third group was given a single dose of d-GalN hydrochloride at the concentration of 500 mg·kg-1 through a saline injection. The final group was given similar concentrations of both the antioxidant combination and d-GalN. Tissue samples were collected under ether anesthesia. The rats treated with d-GalN showed brain damage; increased myeloperoxidase, catalase, glutathione peroxidase, glutathione-S-transferase, lactate dehydrogenase, and superoxide dismutase activities; and decreased glutathione levels. Treatment with vitamins and selenium combination resulted in alleviation of these alterations in the rats. These findings suggest that administration of the vitamins and selenium combination suppresses oxidative stress and protects brain cells from injury induced by d-GalN.