Vitamin C Alleviates Chronic Chlorpyrifos Induced Alterations in Serum Lipids and Oxidative Parameters in Male Wistar Rats

Abstract

Problem statement: Although the increase incidence of cardiovascular diseases, obesity and diabetes mellitus has been attributed to changing life style, the role of environmental contaminants is currently being given considerable attention. Pesticides, including Organophosphate (OP) insecticides are one of the most pervasive environmental contaminants that are deliberately released into the environment. Chlorpyrifos (CPF), a widely used OP insecticide has been shown to alter lipid profiles, thereby increasing the risk of atherosclerosis. Apart from inhibition of acetyl cholinesterase, oxidative stress is one of the molecular mechanisms involved in CPF-evoked toxicity. Approach: The present study was aimed at evaluating the mitigating effect of vitamin C on chronic CPF-evoked alteration in lipid profiles in Wistar rats. Twenty young adult male Wistar rats were assigned at random to four groups of five rats each. Groups I, II and III were administered S/oil (2 mL kg −1 ), vitamin C (100 mg kg −1 ) and CPF (10.6 mg kg −1~1 /8th LD 50 ), respectively while group IV was given vitamin C (100 mg kg −1 ) followed by CPF (10.6 mg kg −1 ), 30 min later. The regimens were administered by gavage once daily for 17 weeks. The sera obtained from blood samples were evaluated for the levels of Cholesterol (TC), Triglycerides (TG), High Density Lipoproteins-Cholesterol (HDL-c), Malonaldehyde (MDA) and the activities of superoxide dismutase and catalase. The levels of low Density Lipoprotein-Cholesterol (LDL-c) and Very Low Density Lipoprotein-Cholesterol (VLDL-c) and atherogenic index, were subsequently calculated. Results: The increased levels of TC, LDL-c, MDA and atherogenic index and the decrease in the levels of TG, HDL-c, VLDL-c, SOD and CAT evoked by CPF were mitigated by vitamin C. Conclusion: It is concluded that vitamin C alleviated the CPF induced deleterious alterations of lipid profiles, partly due to its antioxidant property.

Effect of Dimethoate (An Organophosphate Insecticide) on the Reproductive System and Fertility of Adult Male Rat

“…In mammals, the primary site of action Science Publications AJPT of organophosphate pesticides is the central and peripheral nervous systems and its is by inhibiting acetylcholonesterase, a biochemical event that result in accumulation of endogenous acetylcholine at the nerve endings (Sarkar and Maitra, 1990;Gore, 2001). Several physiological and behavioral dysfunctions occur in animals after exposure to light doses of organophosphate pesticide (Ambali et al, 2011). Thus, the possibility that dimethoate can affect humans and wildlife in their natural habitats is of great concern.…”

Impact of sub-acute exposure to nuvan on serum lipoproteins of catfish, Clarias batrachus and their potential effects indirectly on human health

“…Tanvir et al [34] investigated marked increase in LDL and VLDL with a concomitant reduction in HDL was observed in Chlorpyrifos treated rats [35] and concluded that chlorpyrifos bioaccumulation over time and exerts toxic effects on animals. Additionally, this pattern of change is closely related with a high-risk for coronary artery disease [36] due to the suggestive and antecedent role of LDL oxidation in the pathogenesis of atherosclerosis [37]. Moreover, low HDL may be attributed to nuvan induced hepatic damage, consequently in the impairment of lipoprotein synthesis.…”

Chemopreventive Efficacy of <i>Punica granatum</i> and <i>Silybum marianum </i>Extracts on Chemically-induced Hepatocellular Carcinoma in Rats

“…These results were in accord with the results obtained from earlier studies Hayashi et al [40] ; Taha et al [41] and Adesanoye et al [42] who recorded an elevation in liver enzymes after administration of DEN , CCL4 and AAF. The elevation in serum liver function indices observed in the HCC group could be due to loss of structural integrity of hepatic tissue; liver enzymes are cytoplasmic compartment of hepatocytes; which are liberated to the blood after hepatic degeneration [39].…”