Rutin ameliorates carbon tetrachloride-induced hepatorenal toxicity and hypogonadism.

Rutin ameliorates carbon tetrachloride-induced hepatorenal toxicity and hypogonadism.


PeerJ. 2019 ;7:e7011. Epub 2019 May 29. PMID: 31179192

Abstract Title: 

Rutin ameliorates carbon tetrachloride (CCl)-induced hepatorenal toxicity and hypogonadism in male rats.


Rutin, a food derived-polyphenolic bioflavonoid, has been acknowledged for several health benefits. This study aims to explore the ameliorative effects of rutin against carbon tetrachloride (CCl) toxicity in male rats. Adult male rats were given either CCl(30% in olive oil, 3 ml/kg b.w. intraperitoneally) alone or in combination with rutin (70 mg/kg intragastrically) twice a week for 4 weeks. Our data showed that rutin mitigated CClhepatorenal damage, as indicated by diagnostic markers (i.e., transaminases, alkaline phosphatase, total bilirubin, total protein, albumin, urea, uric acid and creatinine), and histopathological findings. In addition, CClinduced profound elevation of free radical generation and oxidative stress, as evidenced by increasing lipid peroxidation and reducing catalase, superoxide dismutase and glutathione peroxidase activities in liver, kidney and testicular tissues; these effects were suppressed by coexposure with rutin. Moreover, the increase in the levels of serum triglycerides, cholesterol, low-density lipoprotein cholesterol, and very-low-density lipoprotein cholesterol induced by CClwas effectively counteracted by rutin. The decrease in the level of high-density lipoprotein cholesterol in the CClgroup was also counteracted by rutin treatment. Interestingly, the decreased levels of hormonal mediators associated with sperm production, including serum testosterone, luteinizing hormone and follicle-stimulating hormone, and the impaired sperm quality induced by CClwere reversed by rutin. Data from the current study clearly demonstrated that rutin supplementation could at least partly overcome CCl-induced hepatotoxicity, nephrotoxicity and reproductive toxicity by antioxidant and antidyslipidemic effects.

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