Ameliorative potential of α-tocopherol against flubendiamide and copper-induced testicular-insult in Wistar rats

Mandil, Rajesh; Rahal, Anu; Prakash, Atul; Sk, Garg; Gangwar, Neeraj Kumar; Swain, Dilip Kumar

doi:10.1016/j.cbi.2016.11.004

Cited by 19 publications

(18 citation statements)

References 63 publications

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“…It also normalized the spleen histoarchitecture towards almost normal as observed in rats of control groups. This evident ameliorative potential of α-tocopherol is in agreement with our previous findings that studied flubendiamide and copper induced testicular injury [96]. Similar preventive effects of αtocopherol against copper and cadmium-induced cytotoxicity in COS-7 cells [81] and carbofuran-induced genotoxicity in human lymphocytes has also been reported [97].…”

Section: Discussionsupporting

confidence: 92%

In vitro and in vivo effects of flubendiamide and copper on cyto-genotoxicity, oxidative stress and spleen histology of rats and its modulation by resveratrol, catechin, curcumin and α-tocopherol

Mandil¹,

Prakash

Rahal

et al. 2020

BMC Pharmacol Toxicol

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Background: Living organisms are frequently exposed to more than one xenobiotic at a time either by ingestion of contaminated food/fodder or due to household practices, occupational hazards or through environment. These xenobiotics interact individually or in combination with biological systems and act as carcinogen or produce other toxic effects including reproductive and degenerative diseases. Present study was aimed to investigate the cyto-genotoxic effects of flubendiamide and copper and ameliorative potential of certain natural phyotconstituent antioxidants. Method: In vitro cytogenotoxic effects were evaluated by employing battery of assays including Propidium iodide staining, Tunel assay, Micronuclei, DNA fragmentation and Comet assay on isolated splenocytes and their prevention by resveratrol (5 and 10 μM), catechin (10 and 20 μM), curcumin (5 and 10 μM) and α-tocopherol (5, 10 and 20 μM). In vivo study was also undertaken daily oral administration of flubendiamide (200 mg/kg) or copper (33 mg/kg) and both these in combination, and also all these concurrently with of α-tocopherol to Wistar rats for 90 days. Results: Flubendiamide and copper produced concentration-dependent cytotoxic effects on splenocytes and at median lethal concentrations, flubendiamide (40 μM) and copper (40 μM) respectively produced 71 and 81% nonviable cells, higher number of Tunel+ve apoptotic cells, 7.86 and 9.16% micronucleus and 22.90 and 29.59 comets/100 cells and DNA fragmentation. In vivo study revealed significant (P < 0.05) increase in level of lipid peroxidation (LPO) and decrease in glutathione peroxidase (GPx), glutathione-S-transferase (GST) and superoxide dismutase (SOD) activities in groups exposed to flubendiamide or copper alone or both these in combination. Histopathological examination of rat spleens revealed depletion of lymphoid tissue, separation of splenocytes and rarification in splenic parenchyma of xenobiotic(s) treated groups.

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Section: Discussionsupporting

confidence: 92%

In vitro and in vivo effects of flubendiamide and copper on cyto-genotoxicity, oxidative stress and spleen histology of rats and its modulation by resveratrol, catechin, curcumin and α-tocopherol

Mandil¹,

Prakash

Rahal

et al. 2020

BMC Pharmacol Toxicol

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“…Testicular ACP and LDH are regarded as vital markers of spermatogenesis. They are actively involved in the maturation of spermatogenic epithelium, energy metabolism, protein synthesis and metabolism of lactate to ATP during spermatogenesis 51 …”

Section: Discussionmentioning

confidence: 99%

Protective effects of ethyl acetate extract from Shorea roxburghii against diabetes induced testicular damage in rats

Zhao

Olatunji

2020

Environmental Toxicology

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Diabetic mellitus is a chronic metabolic disorder that is associated with several complications including testicular dysfunction. This research investigated the protective action of the ethyl acetate extract from Shorea roxburghii (SRE) on diabetes induced testicular damage in rats. Diabetic rats were orally administered with SRE at doses of 100 and 400 mg/kg for 4 weeks. SRE improved the body weight gain, testes weight, testes index and increased serum concentration of testosterone. Furthermore, SRE increased the testicular antioxidant enzymes including superoxide dismutase, catalase and glutathione peroxidase. In addition, SRE ameliorated testicular inflammatory mediators such as myeloperoxidase, tumor necrosis factor alpha, interleukin 6, p38 MAPK and nuclear factor kappa B activation and decreased testicular cell apoptosis in the treated diabetic rats. SRE also raised sperm parameters after treatment of diabetic rats. Conclusively, our results suggested that SRE ameliorated diabetes induced testicular damage by inhibiting oxidative stress and inflammation.

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“…α-Tocopherol, which exhibits the highest vitamin E bioactivity, has been found to be very effective in ameliorating the toxicity produced by xenobiotics, particularly by reducing oxidative damage in terms of decreased lipid peroxidation and improving the antioxidant system. 39 Unexpectedly, we found that vitamin E treatment did not prevent the MT protein induction, and instead, enhanced the MT protein expression in the DM/VE group. Vitamin E also enhanced the testicular MT protein in the DM/VE group.…”

Section: Discussionmentioning

confidence: 56%

Diabetes Mellitus induces alterations in metallothionein protein expression and metal levels in the testis and liver

Lian

Sun

et al. 2017

J Int Med Res

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ObjectiveTo investigate the effect of diabetes with and without vitamin E treatment on testicular metallothionein (MT) and metal (zinc, copper and iron) changes.MethodsDiabetes was induced with a single intraperitoneal injection (i.p.) of streptozotocin in rats, and diabetic rats were given Vitamin E by i.p. every other day for 4 weeks. MT protein was measured by the cadmium-haeme assay and metal levels were detected by an atomic absorption spectrophotometer.ResultsDiabetes did not change testicular MT protein, but significantly increased hepatic MT protein. Diabetes significantly decreased testicular copper, but not hepatic copper. Zinc and iron levels were unchanged in both diabetic testis and liver. Vitamin E significantly enhanced both testicular and hepatic MT, and zinc levels in diabetic rats. Vitamin E slightly decreased the copper levels, but did not change the testicular and hepatic iron in diabetic rats.ConclusionsTesticular MT protein expression was not increased, even though hepatic MT significantly increased independent of metal changes, in diabetic rats. Vitamin E enhanced testicular and hepatic MT, which correlated with increased zinc levels.

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Ameliorative potential of α-tocopherol against flubendiamide and copper-induced testicular-insult in Wistar rats

Cited by 19 publications

References 63 publications

In vitro and in vivo effects of flubendiamide and copper on cyto-genotoxicity, oxidative stress and spleen histology of rats and its modulation by resveratrol, catechin, curcumin and α-tocopherol

In vitro and in vivo effects of flubendiamide and copper on cyto-genotoxicity, oxidative stress and spleen histology of rats and its modulation by resveratrol, catechin, curcumin and α-tocopherol

Protective effects of ethyl acetate extract from Shorea roxburghii against diabetes induced testicular damage in rats

Diabetes Mellitus induces alterations in metallothionein protein expression and metal levels in the testis and liver

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