Search

The new technological applications of nickel (Ni) raise concerns over its harmful effects on the environment and human health. Pomiferin isolated from Osage orange is evaluated in in vitro and in vivo laboratory bioassays. This study focused the effects of pomiferin on Ni-caused hepatic injury and its underlying mechanisms. With this aim, Sprague-Dawley rats received 10 mg/kg nickel chloride (NiCl 2 ) for 7 d by intraperitoneal injections. Pomiferin was given orally once a day at different doses (75, 150, and 300 mg/kg) for 20 d after exposure to NiCl 2 . Animals were anesthetized and livers were carefully collected to evaluate oxidative stress, inflammation, vascular injury, and hepatic function. Also, immunofluorescence analysis of apoptosis and DNA damage was performed on rat hepatic tissues. NiCl 2 increased MDA production while reducing SOD, CAT, and GPx activity. NiCl 2 induced the production of inflammatory cytokines and also platelet activation in hepatic tissue. Moreover, there were significant increases in AST, ALT, and LDH levels. NiCl 2 also caused significant pathological changes in hepatic. Additionally, it remarkably induced up-regulations of apoptotic marker and 8-OHdG expressions by immunofluorescence labeling in liver cells. Whereas, pomiferin significantly attenuated lipid peroxidation and increased antioxidant defense system in liver. Also, the use of pomiferin prevented deregulated inflammatory process by signaling pathways nuclear factor kappa B (NFκB)/COX-2/TNF-α/IL-1β/IL-6. In addition, pomiferin diminished histopathologic evidence of hepatic toxicity and significantly lower expressions of caspase 3 and 8-OHdG were observed in liver cells. Pomiferin seems to counteract the deleterious effects of NiCl 2 on hepatic tissue through different cellular and signaling mechanisms.

Cisplatin (CP) is an antineoplastic drug; however, owing to its nephrotoxicity, its clinical use is limited. We investigated whether vitexilactone (vitex) is a safe and effective treatment for CP induced kidney injury. We allocated Sprague-Dawley rats into six groups: control group, low dose-high dose vitex groups (40 and 80 mg/kg vitex for 6 days before administration of CP), CP group (single 6 mg/kg dose on day 6) and CP + low dose vitex-CP + high dose vitex group (40 and 80 mg/kg vitex for 6 days, and a single 6 mg/kg dose of CP on day 6. Rats were euthanized 5 days after CP treatment. After exposure to CP and/or vitex, total oxidative stress and total antioxidant status were assessed. The histology of the kidney was examined using hematoxylin and eosin, and periodic acid-Schiff. We used immunohistochemical and fluorescence staining to detect expression of caspase-3. We also measured blood urea nitrogen, uric acid and creatinine levels. Nephroprotective effects of vitex were associated with decreased serum toxicity markers and increased antioxidant activity. Vitex also reduced the expression of the apoptosis marker, caspase-3. Treatment with CP increased blood urea nitrogen, uric acid, creatinine levels and total antioxidant status, and decreased total antioxidant status compared to the control group. Use of vitex for protection from CP induced nephrotoxicity appears to be a safe and efficacious alternative for treatment of kidney injury.

Interleukin-33 (IL-33) is a novel cytokine involved in diabetes mellitus (DM) but its role in diabetic ovarian injury is unknown. As IL-33 is modulated by apoptosis, we aimed at investigating the effect of diabetes on ovaries in terms of evaluating apoptosis and IL-33 in a rat model. In this prospective experimental study, 16 female, nonpregnant Sprague-Dawley albino rats (12 weeks, 220-240 g) were randomly divided into two groups. Group 1 included eight healthy nondiabetic rats as controls and group 2 included eight rats in which diabetes was induced by intraperitoneal (i.p) injection of streptozotocin (STZ). After overt DM occurred (blood glucose >400 mgr/dl), all animals were euthanized and blood samples were collected by cardiac puncture for biochemical analysis. Bilateral oophorectomy was performed for histopathological examination. Serum levels of IL-33 and ovarian IL-33 and caspase-3 immunoexpressions were assessed. Immunoexpressions of caspase-3 and IL-33 were significantly higher in ovarian stromal cells of the diabetic rats compared to the controls. Also, in diabetic group, serum IL33 levels were significantly higher than the control group. In conclusion, increased IL-33 was observed both in serum and ovaries of STZ-induced diabetic rats as well as increased apoptosis in these diabetic rats. IL-33 may contribute to the apoptosis in diabetic ovarian injury.

In this study, we aimed to identify the toxic effects of chlorpyrifos exposure on the tissues of common carp. For this purpose, we evaluated histopathological changes in the brain, gills, liver, kidney, testis, and ovaries after 21 days of chlorpyrifos exposure. Activation of 8-OHdG, cleaved caspase-3, and iNOS were assesed by immunofluorescence assay in chlorpyrifos-exposed brain and liver tissue. Additionally, we measured the expression levels of caspase-3, caspase-8, iNOS, MT1, CYP1A, and CYP3A genes in chlorpyrifos-exposed brain tissue, as well as the expression levels of FSH and LH genes in chlorpyrifos-exposed ovaries, using qRT-PCR. We observed severe histopathological lesions, including inflammation, degeneration, necrosis, and hemorrhage, in the evaluated tissues of common carp after both high and low levels of exposure to chlorpyrifos. We detected strong and diffuse signs of immunofluorescence reaction for 8-OHdG, iNOS, and cleaved caspase-3 in the chlorpyrifos-exposed brain and liver tissues. Furthermore, we found that chlorpyrifos exposure significantly upregulated the expressions of caspase-3, caspase-8, iNOS, and MT1, and also moderately upregulated CYP1A and CYP3A in the brain tissue of exposed carp. We also noted downregulation of FSH and LH gene expressions in chlorpyrifos-exposed ovary tissues. Based on our results, chlorpyrifos toxication caused crucial histopathological lesions in vital organs, induced oxidative stress, inflammation, and apoptosis in liver and brain tissues, and triggered reproductive sterility in common carp. Therefore, we can propose that chlorpyrifos toxication is highly dangerous to the health of common carp. Moreover, chlorpyrifos pollution in the water could threaten the common carp population. Use of chlorpyrifos should be restricted, and aquatic systems should be monitored for chlorpyrifos pollution. [ABSTRACT FROM AUTHOR]

Deltamethrin is a widely used synthetic pyrethroid pesticide that protects agricultural yields, including crops, fruits, and vegetables from insect-pests. It is known that deltamethrin toxication leads to metabolic disorders and has detrimental effects on the brain and liver in different organisms. However, the harmful effects of deltamethrin toxication on aquatic animals remain unclear. In the present study, we aimed to evaluate the adverse effects of deltamethrin toxication by performing a histopathological examination, an immunofluorescence assay, and a qRT-PCR on common carp. We observed that a low-dose (0.04 μM) and a high-dose (0.08 μM) of deltamethrin exposure caused lamellar cells hyperplasia and inflammatory cells infiltration in the gills, hyperemia, diffuse hydropic degenerations and focal necrosis in the hepatocytes, necrotic changes in the neurons, and also induced activation of inducible Nitric Oxide Synthase (iNOS) and 8-hydroxy-2-deoxyguanosine (8-OHdG) in the gills, liver, and brain depending on the exposure time (24 h, 48 h, 72 h and 96 h). In addition, deltamethrin toxication caused the up-regulation of caspase-3 and the inducible Nitric Oxide Synthase (iNOS) of the gene expression depending on the dose (0.04 μM and 0.08 μM) and the exposure time in the brain ( p < 0.05, p < 0.01, p < 0.001 ). Our results indicated that long-term deltamethrin exposure could lead to inflammation, oxidative stress, DNA damage, and apoptosis on the different organs in common carp. Thus, deltamethrin toxication is dangerous for common carp populations, and the usage of deltamethrin should be controlled and restricted in agricultural areas. [ABSTRACT FROM AUTHOR]

ABSTRACT Cisplatin (CP) treatment causes the damage in male reproductive system. Carvacrol (CARV) is an antioxidant that is naturally found in some plants. We aimed to investigate the effect of CARV on CP-induced reproductive toxicity in male rats. Eighteen adult male Sprague-Dawley rats were used. The control group ( n = 6) was treated orally with physiological saline (PS) daily for 14 days and a single intraperitoneal (IP) PS injection on day 10. The CP group ( n = 6) was administered with daily oral PS for 14 days and a single IP injection of 10 mg/kg CP on day 10. The CARV + CP group ( n = 6) was treated with daily 75 mg/kg oral CARV for 14 days and a single IP injection of 10 mg/kg CP on day 10. CP treatment caused the damage on some spermatological parameters (motility, live sperm rate, and abnormal sperm rate), increased the oxidative stress, and induced testicular degeneration and apoptosis. However, CARV treatment mitigates CP-induced reproductive toxicity. [ABSTRACT FROM AUTHOR]

Cypermethrin (Cyp), a known neurotoxic pesticide, is widely used in agricultural applications. In the present study, the aim was to determine the histopathological effects of Cyp toxication and evaluate the activation of inducible nitric oxide synthetase (iNOS) and 8-hydroxy-2-deoxyguanosine (8-OHdG) using an immunofluorescence assay. Thereafter, we identified the expressions of caspase 3, capsase 8, iNOS, and metallothionein 1 (MT1) genes in common carp using quantitative reverse transcription polymerase chain reaction (qRT-PCR). High and low doses of Cyp were administered to experimental groups for 24, 48, 72, and 96 h. As a result, necrotic neurons in different stages and desquamation of ependymal cells due to necrosis were detected in the brain. Histopathological changes, including hyperplasia of lamellar cells, telangiectasia of lamellae and thickening due to cellular infiltration in gills, hemorrhage, diffuse hydropic degeneration, and focal necrosis in the liver were observed in the experimental groups. Immunopositive reactions of 8-OHdG were clearly observed in the nuclei and cytoplasm of neurons, and positive reactions for iNOS were detected in the cytoplasm of neurons and in the glial cells of the experimental groups. Furthermore, we found that caspase 3, capsase 8, iNOS, and MT1 genes were up-regulated in the brain when exposed to both high and low doses of Cyp. In conclusion, our findings revealed that Cyp toxication harms the organs of common carp, particularly the brain, and also gives rise to inflammation, DNA damage, and apoptosis. Therefore, the use of Cyp should be restricted to protect the health of aquatic animals. [ABSTRACT FROM AUTHOR]

In this study, our aim was to evaluate lesions seen in the tissues in terms of histopathology and to investigate the apoptotic cells seen in the tissues when E. coli outbreak occurred in a poultry farm. A total of 48 Lohmann White strains (53 weeks old) were submitted to the laboratory for necropsy. Microbiologic and histopathologic examinations were done on the samples taken from tissues. Apoptotic cells were determined in all of the tissues. The number of apoptotic cells increased as the tissue damage increased. [ABSTRACT FROM AUTHOR]