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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

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.

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.

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

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.

Metformin is a biguanide derivate used as an oral hypoglycaemic drug in diabetics. The aim of this study was to examine the histological and biochemical effects of metformin in streptozotocin (STZ)-treated rats. The animals were rendered diabetic by intraperitoneal injection of 65 mg/kg STZ. Fourteen days later, metformin was given at 25 mg/kg by gavage, daily for 28 days, to STZdiabetic rats and a control group. In the STZ-diabetic group, some degenerative changes were observed by light microscopic examination. But the degenerative changes were decreased in the STZ-diabetic group given metformin. In the STZ-diabetic group, blood glucose levels, serum alanine and aspartate transaminase (ALT and AST) activities, total lipid levels, and sodium and potassium levels increased, while body weight, serum magnesium levels and liver glutathione (GSH) levels decreased. In the STZ-diabetic group given metformin, blood glucose levels, serum ALT and AST activities, total lipid, and sodium and potassium levels decreased, and liver GSH and serum magnesium levels increased. As a result of all the morphological and biochemical findings obtained, it was concluded that metformin has a protective effect against the hepatotoxicity produced by STZ diabetes.

Parsley is used by diabetics in Turkey to reduce blood glucose. The present study aims to investigate both the morphological and biochemical effects of parsley on liver tissue. Rat hepatocytes were examined by light and electron microscopy. Degenerative changes were observed in the hepatocytes of diabetic rats. These degenerative changes were significantly reduced or absent in the hepatocytes of diabetic rats treated with parsley. Blood glucose levels, alanine transaminase and alkaline phosphatase were observed to be raised in diabetic rats. Diabetic rats treated with parsley demonstrated significantly lower levels of blood glucose, alanine transaminase and alkaline phosphatase. The present study suggests that parsley demonstrates a significant hepatoprotective effect in diabetic rats.

Chard (Beta vulgaris L. var cicla) is one of the medicinal herbs used by diabetics in Turkey. It has been reported to reduce blood glucose. We have investigated the effect of chard extracts on the liver by biochemical and morphological investigation. The plant extract was administered by the gavage technique to rats at a dose of 2 g/kg every d for 28 d, 14 d after experimental animals were made diabetic. In the diabetic group, some degenerative changes were observed by light and electron microscope examination, but degenerative changes decreased or were not observed in the diabetic group given chard. In the diabetic group, blood glucose levels, serum alanine, aspartate transaminase, alkaline phosphatase activities, total lipids, sialic and uric acid levels, liver lipid peroxidation (LPO), and nonenzymatic glycosylation (NEG) levels increased, while blood glutathione, body weight, and liver glutathione (GSH) levels decreased. The diabetic group given chard, serum alanine, aspartate transaminase, alkaline phosphatase activities, total lipid level, sialic and uric acid levels, blood glucose levels, and liver LPO and NEG levels decreased, but the other values increased. As a result of all the morphological and biochemical findings obtained, it was concluded that the extract of this plant has a protective effect on the liver in diabetes mellitus.

The aim of this work was to investigate the biochemical and histological effects of vanadyl sulfate on blood glucose, urea, and creatinine in serum and nonenzymatic glycosylation and glutathione levels in kidney tissue of normal and streptozotocin (65 mg/kg) diabetic rats. Vanadyl sulfate was administered by gavage at a dose of 100 mg/kg. After 60 d of treatment, serum urea, creatinine, and blood glucose levels significantly increased in the diabetic group but not so in the vanadyl sulfate, which showed significantly reduced serum urea and blood glucose levels and a nonsignificant reduction of serum creatinine levels. Nonenzymatic glycosylation was increased and the glutathione level was decreased in the kidney tissue of diabetic rats. Treatment with vanadyl sulfate reversed these effects. Degenerative changes were detected in diabetic animals by electron and light microscopy. Although there are individual differences in diabetic animals given vanadium, some reduction of degenerative changes were observed.

The aim of this work was to investigate the effects of chard (Beta vulgaris L. var. cicla) extract on serum urea and creatinine concentrations and on kidney tissue in normal and streptozotocin-diabetic rats. The extract was administered to rats at a dose of 2 g/kg every day for 28 days, 14 days after animals were made diabetic. On day 42, kidney tissue and blood samples were examined. Significant degenerative changes in kidney tissue of diabetic rats were observed, but in the group given chard extract, the morphology of kidney tissue was found to be nearly the same as the controls. Serum urea and creatinine levels significantly increased in the diabetic groups, but the chard extracts significantly reduced serum urea and creatinine levels. It is concluded that the extract of this plant may reduce serum urea and creatinine levels and confer a protective effect on the kidney of diabetic rats.

Aluminum has toxic potential on humans and animals when it accumulates in various tissues. It was shown in a number of studies that aluminum causes oxidative stress by free radical formation and lipid peroxidation in tissues and thus may cause damage in target organs. Although there are numerous studies investigating aluminum toxicity, biochemical mechanisms of the damage caused by aluminum have yet to be explained. Melatonin produced by pineal gland was shown to be an effective antioxidant. Since kidneys are target organs for aluminum accumulation and toxicity, we have studied the role of melatonin against aluminum-induced renal toxicity in rats. Wistar albino rats were divided into five groups. Group I served as control, and received only physiological saline; group II served as positive control for melatonin, and received ethanol and physiological saline; group III received melatonin (10 mg/kg); group IV received aluminum sulfate (5 mg/kg) and group V received aluminum sulfate and melatonin (in the same dose), injected three times a week for 1 month. Administration of aluminum caused degenerative changes in renal tissues, such as increase in metallothionein immunoreactivity and decrease in cell proliferation. Moreover, uric acid and lipid peroxidation levels and xanthine oxidase activity increased, while glutathione, catalase, superoxide dismutase, paraoxonase 1, glucose-6-phosphate dehydrogenase, and sodium potassium ATPase activities decreased. Administration of melatonin mostly prevented these symptoms. Results showed that melatonin is a potential beneficial agent for reducing damage in aluminum-induced renal toxicity.

Diabetes Mellitus is a lifelong chronic metabolic disease, requiring continuous follow-up and therapy, it reduces the quality of life of patients with acute and chronic complications, mortality, and its economic burden is high. Cancer is the second cause of death, according to World Health Organization data. Prostate cancer is one of the most common cancers in the developed world and the second leading cause of male cancer related death. As with other cancer types, metastasis is an essential problem that we are facing and it is not clear whether a tumor will metastasize or not in localized state. It has been reported that there are high levels of voltage-gated sodium channels in metastatic prostate cancer cases. Cancer, ever growing with diabetes, is a major health problem. Studies have shown that diabetic patients have higher cancer rates than those of non-diabetics . Metformin is the drug of choice for the treatment of diabetes. Recently, there are studies in the literature regarding metformin reducing the risk of cancer besides its effect on diabetes This review will explain the possible role of the metformin on the three dimensional relationship of prostate cancer, diabetes andion channels, and provide a significant contribution to clinical trials. Keywords: Cancer, experimental diabetes, metformin, voltage gated sodium channel, MAT-Lylu cells

The aim of this study was to determine whether vitamin C, vitamin E, and selenium have protective effects against cadmium-induced renal toxicity of rats. Vitamin C (250 mg/kg/day), vitamin E (250 mg/kg/day), and sodium selenate (0.25 mg/kg/day) were given to rats orally for 8 days. Cadmium (2 mg/kg/day CdCl2) was given to rats intraperitoneally. Vitamin C, vitamin E, and selenium (in the same dose and time) were given 1 h prior to the administration of cadmium every day. The tissue and blood samples were taken from the rats for histological evaluation and biochemical analyses on the Day 9. Lipid peroxidation (LPO) and glutathione (GSH) determination were made in kidney tissue. In addition, urea and creatinine levels were determined in serum. The damage to the kidney tissue was moderate in the rats given cadmium. In this group, the distinctive changes in the proximal tubules were observed. Degenerative changes in kidney tissue were also observed in rats given vitamin C, vitamin E, selenium, and cadmium. LPO levels significantly increased and GSH levels decreased in kidney tissues following cadmium administration. Serum urea and creatinine levels were also increased in rats given cadmium. The administration of vitamin C, vitamin E, and selenium caused a significant decrease in LPO levels and an increase in GSH levels in the kidney of rats given cadmium. Serum urea and creatinine levels were decreased in rats given both the antioxidant and cadmium. It is concluded that vitamin C, vitamin E, and selenium showed some protective effect on the rat kidney.

In this study, the effects of Melissa officinalis L. extract on hyperlipidemic rats were investigated, morphologically and biochemically. The animals were fed a lipogenic diet consisting of 2% cholesterol, 20% sunflower oil and 0.5% cholic acid added to normal chow and were given 3% ethanol for 42 days. The plant extract was given by gavage technique to rats to a dose of 2 g/kg every day for 28, 14 days after experimental animals done hyperlipidemia. The degenerative changes were observed in hyperlipidemic rats, light and electron microscopically. There was a significant increase in the levels of serum cholesterol, total lipid, alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP), a significant decrease in the levels of liver tissue glutathione (GSH), a significant increase in the levels of tissue lipid peroxidation (LPO) in this group. On the other hand, the administration of Melissa officinalis L. extract reduced total cholesterol, total lipid, ALT, AST and ALP levels in serum, and LPO levels in liver tissue, moreover increased glutathione levels in the tissue. As a result, it was suggested that Melissa officinalis L. extract exerted an hypolipidemic effect and showed a protective effect on the liver of hyperlipidemic rats.

Glibornuride is a sulphonylurea derivative used as an oral hypoglycaemic drug in diabetics. The aim of this study was to examine the histological, ultrastructural and biochemical effects of glibornuride in streptozotocin (STZ)-treated rats. The animals were rendered diabetic by intraperitoneal injection of 65 mg/kg STZ. Fourteen days later, glibornuride was given at 5 mg/kg by gavage, daily for 28 days, to one STZ-diabetic and one control group. In the STZ-diabetic group, remarkable degenerative changes were observed. On the other hand, in the STZ-diabetic group given glibornuride, the degenerative changes decreased. In the STZ-diabetic group, blood glucose levels, serum aspartate transaminase activity, and total lipid levels increased, whereas the blood glutathione levels decreased. In contrast, in the STZ-diabetic group given glibornuride blood glucose levels, serum aspartate transaminase activity and total lipid levels decreased and blood glutathione levels increased. Significant changes in total protein levels in the serum were not observed in any group. As a conclusion, we can say that glibornuride has a protective effect against the hepatotoxicity produced by STZ-diabetes.