Hepatotoxicity of graphene oxide in Wistar rats.

Graphene oxide (GO) has a multitude of applications in areas of nanomedicine, electronics, textile, water purification, and catalysis among others. GO is relatively easier to manufacture and customize as compared with other carbon-based nanomaterials. In the present work, GO was administered intraperitoneally to adult Wistar rats in four incremental doses, i.e., 0.0 mg/kg (control), 0.4 mg/kg (low dose), 2.0 mg/kg (mid-dose), and 10.0 mg/kg (high dose). After 15 repeated doses over a period of 30 days, biochemical assays for alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), catalase (CAT), and malondialdehyde (MDA) were carried out. Histopathological and morphometric analyses of liver and kidney were also performed. Results demonstrated dose-dependent toxicity of GO. General behavior and liver indices remained unaffected in the study. Serum levels of ALT, ALP, and AST were altered significantly in high-dose treated animals. Changes were found insignificant in the low- and mid-dose groups. Catalase activity in liver tissue homogenates was decreased in the high-dose group. MDA levels were found elevated in treated rats. Unlike control and low dose, mid- and high-dose treated rats exhibited varying degrees of histopathological changes like inflammation around the central vein and portal veins, vacuolations, hepatocytic injury, and near normal to abnormal hepatic sinusoids. These findings show that GO has considerable toxic potential to mammalian liver and thorough toxicity studies are needed before these nanosheets are used in biomedicine.

Bifenthrin-induced neurotoxicity in rats: involvement of oxidative stress.

Extensive use of synthetic pyrethroids has resulted in serious human health issues. Induction of oxidative stress is an important mechanism of action of most pesticides including pyrethroids. In the present study, we have elucidated the possible role of oxidative stress in bifenthrin-induced neurotoxicity. Adult male Wistar rats were administered bifenthrin (3.5 and 7 mg per kg body weight p.o.) for 30 days. Behavioral studies were conducted on a set of randomly selected rats from each treatment group after completion of treatment. Neurochemical parameters were assessed 24 h after the last dose was administered. The selected behavioral and neurochemical endpoints were also assessed 15 days after cessation of exposure to reveal whether the neurobehavioral changes produced by bifenthrin were temporary or permanent. Deficits in motor activity, motor incoordination, and cognitive impairment were observed after exposure to bifenthrin. Levels of biogenic amines viz. dopamine (DA) and its metabolites, i.e. 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), epinephrine (EPN), norepinephrine (NE), and serotonin (5-HT) altered in the frontal cortex, corpus striatum, and hippocampus of bifenthrin-treated rats. A decrease in the activity of acetylcholinesterase (AChE) occurred in all regions of the brain. Both doses of bifenthrin significantly induced lipid peroxidation (LPO) and increased protein carbonyl levels in the frontal cortex, corpus striatum, and hippocampus of rats. The activities of antioxidant enzymes, i.e. catalase, superoxide dismutase, and glutathione peroxidase, were also suppressed in all selected regions of the brain. A trend of recovery was, however, observed in all the behavioral and neurochemical endpoints 15 days after withdrawal of exposure. Oxidative stress seems to play an important role in bifenthrin-induced neurotoxicity. Our study suggests that long-term exposure to these compounds can produce detrimental effects.