Methomyl-induced nephrotoxicity and protective effect of curcumin in male rats.

We investigated the ameliorative effect of the curcumin against methomyl-induced potential nephrotoxicity in Wistar albino male rats. In the present study, curcumin (100 mg kg-1 bw), methomyl (0,8 mg kg-1 bw) and methomyl plus curcumin were given to rats by oral for 28 days (for subacute examination). Concentrations of blood urea nitrogen, uric acid and creatinine in serum and malondialdehyde level and activities of antioxidant enzyme (superoxide dismutase, catalase, glutathione peroxidase and glutathione S transferase) and histopathological alterations in kidney tissues were studied. Methomyl caused an increment in the concentrations of blood urea nitrogen, creatinine, uric acid and MDA levels. In addition, methomyl caused a diminution in the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione S transferase. Tubular and glomerular degenerations occurred in the kidney tissues of methomyl-received rats. However, coadministration of curcumin with methomyl significantly minimized the adverse effects of methomyl on kidney function parameters, lipid peroxidation and antioxidant enzyme activities and histological structure of kidney tissue. The results showed that curcumin significantly mitigated methomyl-induced nephrotoxicity in rats.

Protective potential of curcumin or taurine on nephrotoxicity caused by bisphenol A.

Bisphenol A (BPA) received heightened attention in the recent years due to humans continuously being exposed to it. This study explores the effect of taurine or curcumin on subacute BPA treatment-induced nephrotoxicity in rats (Rattus norvegicus). Forty-two adult albino male rats were exposed to BPA (130 mg/kg daily) for 28 days by gastric gavage. BPA led to lipid peroxidation, inhibiting antioxidant enzyme activities like catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione S-transferase (GST). BPA exposure also induced histopathological changes like tubular and glomerular degeneration, vascular congestion, and interstitial cell infiltration in kidney tissue. Cotreatment with taurine (100 mg/kg daily) or curcumin (100 mg/kg daily) alleviated the lipid peroxidation level and antioxidant enzyme activities and histological alterations brought about by BPA. In this study, curcumin and taurine application provided protection against renal toxicity caused by BPA but did not prevent toxic effect completely.

Hepatoprotective effects of curcumin and taurine against bisphenol A-induced liver injury in rats.

Bisphenol A (BPA) is an estrogenic endocrine disrupting chemical to which humans are frequently exposed during routine daily life. Curcumin and taurine are natural products that have also been used as antioxidants against different environmental toxin-induced hepatotoxicity. Furthermore, they have protective and therapeutic effects against various diseases. The present investigation has been conducted to evaluate the therapeutic potential of curcumin (100 mg kg-1) and taurine (100 mg kg-1) for their hepatoprotective efficacy against BPA (130 mg kg-1)-induced liver injury in rat. BPA significantly elevated the levels of malondialdehyde (MDA), while it reduced the activities of catalase (CAT), total glutathione S-transferase (GST), total glutathione peroxidase (GPx), and total superoxide dismutase (SOD). Besides, these biochemical changes were accompanied by histopathological alterations marked by the destruction of normal liver structure. The histological examinations showed that exposure of BPA caused dilatation of sinusoids, inflammatory cell infiltration, congestion, and necrosis in liver parenchyma. The BPA-induced histopathological alterations in liver were minimized by curcumin and taurine treatment. Furthermore, no necrosis was observed in the liver tissues of curcumin plus BPA and taurine plus BPA-treated rats. Oral administration of curcumin and taurine to BPA-exposed rats significantly reversed the content of lipid peroxidation products, as well as enhanced the activities of GPx and GST, CAT, and SOD enzymes. These findings have indicated that curcumin and taurine might have a protective effect against BPA-induced hepatotoxicity in rats.

Histopathological and biochemical studies on the effect of curcumin and taurine against bisphenol A toxicity in male rats.

Bisphenol A (BPA) is a chemical found in environmental xenoestrogen. In the present study, olive oil, curcumin, taurine, BPA, curcumin plus BPA, and taurine plus BPA were exposed to rats for 4 weeks via gavage. Content of malondialdehyde and activities of antioxidant enzymes (GPx, GST, SOD, CAT) and also histopathological and cytopathological changes of heart were studied. No significant changes in all studied parameters were seen between control, olive oil, curcumin, and taurine-treated groups. However, there were significant differences in levels of malondialdehyde and activities of antioxidant enzymes in BPA-exposed rats and some histo/cytopathological changes determined. In curcumin plus BPA-exposed and taurine plus BPA-exposed groups, we measured the preventive effects on some parameters but not exactly. As a result, curcumin and taurine significantly minimized BPA-induced cardiotoxicity in rats.

Mercuric chloride induced hepatotoxic and hematologic changes in rats: The protective effects of sodium selenite and vitamin E.

This study focuses on investigating the possible protective effect of sodium selenite (Na2SeO3) and/or vitamin E against mercuric chloride (HgCl2)-induced hepatotoxicity in rat. Male rats were given HgCl2 (1 mg/kg body weight (bw)) and HgCl2 plus Na2SeO3 (0.25 mg/kg bw) and/or vitamin E (100 mg/kg bw) daily via gavage for 4 weeks. HgCl2-treated groups had significantly higher white blood cell and thrombocyte counts than the control group. Serum activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, γ-glutamyl-transferase, and lactate dehydrogenase significantly increased and serum levels of total protein, albumin, triglyceride, total cholesterol, and low-density lipoprotein cholesterol significantly decreased in the HgCl2-treated groups compared with control group. Malondialdehyde level significantly increased and superoxide dismutase, catalase, and glutathione peroxidase activities decreased in liver tissue of HgCl2-treated rats. Also, HgCl2 exposure resulted in histopathological changes. Supplementation of Na2SeO3 and/or vitamin E provided partial protection in hematological and biochemical parameters that were altered by HgCl2 As a result, Na2SeO3 and/or vitamin E significantly reduced HgCl2-induced hepatotoxicity, but not protected completely.

Vitamin E and Sodium Selenite Against Mercuric Chloride-Induced Lung Toxicity in the Rats

The aim of the present study was to elucidate the possible protective role of vitamin E and / or sodium selenite on mercuric chloride-induced oxidative stress and histopathological changes in the lung tissue of the rats. Adult male albino Wistar rats were exposed to mercuric chloride (1.0 mg/kg day) for four weeks. Treatment with mercuric chloride led to oxidative stress by enhancing MDA level and also decreasing superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) and glutathione S transferaz (GST) activities. However, mercuric chloride exposure resulted in histopathological changes in the lung tissue in the rats. MDA level and SOD, CAT GPx and GST activities and histopathological changes modulated in concomitantly supplementation of vitamin E (100 mg/kg day) and /or sodium selenite (0.25 mg/kg day) to mercuric chloride-treated groups.

Sodium selenite and vitamin E in preventing mercuric chloride induced renal toxicity in rats.

This study aims to investigate improving effects of sodium selenite and/or vitamin E on mercuric chloride-induced kidney impairments in rats. Wistar male rats were exposed either to sodium selenite (0.25mg/kgday), vitamin E (100mg/kgday), sodium selenite+vitamin E, mercuric chloride (1mg/kgday), sodium selenite+mercuric chloride, vitamin E+mercuric chloride and sodium selenite+vitamin E+mercuric chloride for 4weeks. Mercuric chloride exposure resulted in an increase in the uric acid, creatinine, blood urea nitrogen and malondialdehyde (MDA) levels and a decrease in the superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities. Histopathological changes were detected in kidney tissues in mercuric chloride-treated groups. A significant decrease in the uric acid, creatinine, blood urea nitrogen and MDA levels and a significant increase in the SOD, CAT and GPx activities were observed in the supplementation of sodium selenite and/or vitamin E to mercuric chloride-treated groups. Conclusively, sodium selenite, vitamin E and vitamin E+sodium selenite significantly reduce mercuric chloride induced nephrotoxicity in rats, but not protect completely.

Mercuric chloride-induced testicular toxicity in rats and the protective role of sodium selenite and vitamin E.

Mercury has been recognized as an environmental pollutant that adversely affects male reproductive systems of animals. This study examined the effects of mercuric chloride on the antioxidant system and histopathological changes and also evaluated the ameliorating effects of sodium selenite and/or vitamin E in the rat testis tissues. Sexually mature male Wistar rats (weighing 300-320g and each group six animals) were given mercuric chloride (1mg/kg bw) and/or sodium selenite (0.25mg/kg bw)+vitamin E (100mg/kg) daily via gavage for 4weeks. In the present study, mercuric chloride exposure resulted in an increase in the TBARS level and a decrease in the SOD, CAT, GPx activities, with respect to the control. Further, light microscopic investigation revealed that mercury exposure induced histopathological alterations in the testis tissues. Supplementation of sodium selenite and/or vitamin E to mercury-induced groups declined lipid peroxidation, increased SOD, CAT, GPx activities. While some histopathological changes were detected in mercuric chloride treated group, milder histopathological changes were observed in animal co-treated with sodium selenite and/or vitamin E supplementation to mercuric chloride-treated rats. As a result, mercuric chloride induced testicular toxicity is reduced by sodium selenite and/or vitamin E, but not ameliorate completely.