The current study investigated the effects of deltamethrin, fluoride (F(-)) and their combination on the hepatic oxidative stress and consequent alterations in blood biochemical markers of hepatic damage in rats. Significant hepatic oxidative stress and hepatic damage were observed in the toxicant exposed groups. These changes were higher in the deltamethrin-F(-) co-exposure treatment group, depicting a positive interaction between the two chemicals.

Sub-acute Deltamethrin and Fluoride Toxicity Induced Hepatic Oxidative Stress and Biochemical Alterations in Rats

Cypermethrin and beta-cyfluthrin are two most widely used multipurpose pyrethroids. After determining their oral LD50 (416.98 mg kg-1 and 354.8 mg kg-1 body weight, respectively), we assessed their hepatotoxicity in Wistar rats following acute (0.1 LD50 for 1 day) and sub-acute (0.1 LD50 for 7, 14, 21 or 28 days) poisoning. The assessment was based on hepatic marker enzymes AST, ALT, LDH, ALP, glycogen, total proteins, total lipids, cholesterol, free fatty acids, and phospholipids. AST, ALT, LDH, total lipids, cholesterol, phospholipids, and free fatty acids in hepatic homogenate increased following pyrethroid stress. In contrast, hepatic proteins, glycogen, and ALP activity decreased due to lysis of structural proteins and leakage of enzymes into the blood stream. Biochemical data were consistent with histological alterations (cytoplasmic vacuolisation, nuclear polymorphism, eccentric nucleus, karyolysis, karyorrhexis, and sinusoidal dilation). Comparatively greater hepatocellular damage was noted in beta-cyfluthrin than in cypermethrin-treated rats, which is probably related to the fluorine atom in beta-cyfluthrin.

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Biochemical and Histological Changes in Rat Liver Caused by Cypermethrin and Beta-Cyfluthrin

The oxidative stress-inducing potential of the pyrethroid insecticide, bifenthrin, was evaluated in rats at 5.8 mg/kg body weight once daily for 20 or 30 days. Bifenthrin treated animals showed significantly increased lipid peroxidation, evidenced by increased blood malondialdehyde levels. Blood glutathione levels and activities of catalase and glutathione peroxidase decreased significantly in the bifenthrin treated animals after both 20 and 30 days of treatment, whereas, the activities of superoxide dismutase and glutathione S-transferase decreased significantly only on the 30th day. In conclusion, bifenthrin has a potential to induce severe oxidative stress in rats exposed to sublethal concentrations.

Effect of repeated oral administration of bifenthrin on lipid peroxidation and anti-oxidant parameters in Wistar rats.

Fenpropathrin induces testicular damage, apoptosis, and genomic DNA damage in adult rats: Protective role of camel milk

This study was designed to investigate the possibility of β-cyfluthrin to induce oxidative stress and biochemical perturbations in rat liver and the role of selenium in alleviating its toxic effects. Male Wister rats were randomly divided into four groups of seven each, group I served as control, group II treated with selenium (200 µg/kg BW), group III received β-cyfluthrin (15 mg/kg BW, 1/25 LD50 ), and group IV treated with β-cyfluthrin plus selenium. Rats were orally administered their respective doses daily for 30 days. The administration of β-cyfluthrin caused elevation in lipid peroxidation (LPO) and reduction in the activities of antioxidant enzymes including catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione peroxidase (GPx), and glutathione reductase (GR). A decrease in reduced glutathione (GSH) content was also observed. Liver aminotransferases (AST and ALT) and alkaline phosphatase (ALP) were decreased, whereas lactate dehydrogenase (LDH) was increased. Selenium in β-cyfluthrin-induced liver oxidative injury of the rats modulated LPO, CAT, SOD, GSH, GST, GPx, and GR. Also, liver AST, ALT, ALP, and LDH were maintained near normal level due to selenium treatment. It is concluded that selenium scavenges reactive oxygen species and render a protective effect against β-cyfluthrin toxicity.

Selenium modulates β-cyfluthrin-induced liver oxidative toxicity in rats

Beta-Cyfluthrin is one of the most widely used type-II pyrethroid in agriculture. Toxic effects of beta-cyfluthrin are due to the presence of cyano moiety in its chemical structure. This study was designed the effect of betacyfluthrin at different doses on brain tissue, the most important vital organ in animal body and in which dose level beta-cyfluthrin shows its effects. Animal were initially divided into control and beta-cyfluthrin given groups. There were five animals in the control group and twenty five animals in beta-cyfluthrin administered group. The latter was divided into five equal subgroups: 35.48, and 5.06, 2.53, 1.68, 1.27mg/kg body weight of beta-cyfluthrin administered groups, acute (1 day) and sub-acute (7, 14, 21 and 28 days) by gavage respectively. Control group was given only water. The effect of these treatments were studied on activities of four potential biomarkers were assayed in the brain of albino rat along with neurosomatic index viz. Body weight, brain weight and brain weight body weight ratio and neurobehavioural changes. Beta-cyfluthrin treatment resulted in a significant decrease in brain acetyl-cholinesterase. Acetylcholinesterase which found to be decreased (inhibition range 53 to 18%) in albino rats after acute and sub-acute treatment (vide-supra). Further glutathione-s-transferase (GST) was also found to be decreased in brain of albino rats (inhibition range 47 to29%) after beta-cyfluthrin administration. Again brain adenosine triphosphtase (total ATPase) activity was seen to decrease in albino rats (inhibition range 36 to19%) along with succinic dehydrogenase (SDH) was also seen decreased in brain of albino rats (inhibition range 31 to 9%)) after acute and sub-acute beta-cyfluthrin intoxication. Further hypnoatremia (inhibition range 31 to 20%) along with hypokalemia (inhibition range 19 to 14%) has also been observed after acute and sub-acute intoxication of beta-cyfluthrin. Apart from AChE, which is a specific marker of pyrethroid neurotoxicity, the levels of brain GST, ATPase, SDH along with Na and K may serve as important determinants of beta-cyfluthrin induced neuronal dysfunctioning along with neurobehavioural alterations; outcomes of fluctuated brain biochemistry because clinical signs of toxicity were observed in animals which received different doses of beta-cyfluthrin after 7 th , and 14 th days of sub-acute treatment. Animals showed overt cholinergic signs which included salivation, excitability, ataxia, muscle twisting, followed by general tremors and lethargyness. The treated groups did not reveal any mortality. Exposure of animals to beta-cyfluthrin caused extensive changes in neurosomatic, neurochemical and neurobehavioural parameters. So, oral administration of beta-cyfluthrin leads to negative response on animal health.

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HN Sharma

Papers

Stress induced by beta-cyfluthrin, a type-2 pyrethroid, on brain biochemistry of Albino rat (Rattus norvegicus)