Cypermethrin (CYP), a synthetic pyrethroid is a common environmental toxicant owing to its wide usage as a broad-spectrum insecticide. Its exposure to non-target organisms, including man, elicits numerous adverse effects making it a major public health issue. Epicatechin (EC) has proven anti-oxidative and anti-inflammatory properties. The present study was undertaken to evaluate the protective efficacy of epicatechin with regards to altered oxidative and inflammatory parameters subsequent to CYP treatment in rats. Animals were divided into four groups. The first group served as the control, while groups 2, 3, and 4 were orally treated with EC (30 mg kg À1 body weight), CYP (25 mg kg À1 body weight), and CYP plus EC, respectively. Oral administration of CYP for 14 days increased the levels of oxidative stress markers such as malondialdehyde, lipid hydroperoxides, and advanced oxidized protein products in the liver and kidney. These were accompanied by a decrease in glutathione and total antioxidant capacity levels. The activity of the enzyme superoxide dismutase was increased while catalase and glutathione peroxidase activities were decreased in these organs. Moreover, CYP increased plasma levels of the pro-inflammatory cytokines, interleukin-6 and tumor necrosis factor alpha. The plasma content of the nitrative nucleic acid marker, 8-nitroguanine was also markedly elevated by CYP. Administration of EC to CYPexposed rats mitigated the induced oxidative and inflammatory effects. These data suggest that EC can attenuate the toxic effects induced by CYP exposure.

BackgroundRecent epidemiological evidences indicate close association between inorganic arsenic exposure via drinking water and cardiovascular diseases. However, the exact mechanism of this arsenic-mediated increase in cardiovascular risk factors remains enigmatic.MethodsIn order to investigate the effects of inorganic arsenic exposure on lipid metabolism, male albino rats were exposed to 50, 100 and 150 ppm arsenic as sodium arsenite and 100, 150 and 200 ppm arsenic as sodium arsenate respectively in their drinking water for 12 weeks.ResultsDyslipidemia induced by the two arsenicals exhibited different patterns. Hypocholesterolemia characterised the effect of arsenite at all the doses, but arsenate induced hypercholesterolemia at the 150 ppm As dose. Hypertriglyceridemia was the hallmark of arsenate effect whereas plasma free fatty acids (FFAs) was increased by the two arsenicals. Reverse cholesterol transport was inhibited by the two arsenicals as evidenced by decreased HDL cholesterol concentrations whereas hepatic cholesterol was increased by arsenite (100 ppm As), but decreased by arsenite (150 ppm As) and arsenate (100 ppm As) respectively. Brain cholesterol and triglyceride were decreased by the two arsenicals; arsenate decreased the renal content of cholesterol, but increased renal content of triglyceride. Arsenite, on the other hand, increased the renal contents of the two lipids. The two arsenicals induced phospholipidosis in the spleen. Arsenite (150 ppm As) and arsenate (100 ppm As) inhibited hepatic HMG CoA reductase. At other doses of the two arsenicals, hepatic activity of the enzyme was up-regulated. The two arsenicals however up-regulated the activity of the brain enzyme. We observed positive associations between tissue arsenic levels and plasma FFA and negative associations between tissue arsenic levels and HDL cholesterol.ConclusionOur findings indicate that even though sub-chronic exposure to arsenite and arsenate through drinking water produced different patterns of dyslipidemia, our study identified two common denominators of dyslipidemia namely: inhibition of reverse cholesterol transport and increase in plasma FFA. These two denominators (in addition to other individual perturbations of lipid metabolism induced by each arsenical), suggest that in contrast to strengthening a dose-dependent effect phenomenon, the two forms of inorganic arsenic induced lipotoxic and non-lipotoxic dyslipidemia at “low” or “medium” doses and these might be responsible for the cardiovascular and other disease endpoints of inorganic arsenic exposure through drinking water.

The present study was designed to investigate aluminium phosphide (ALP)-induced testicular toxicity, including its effects on sperm parameters and histological alterations in Wistar rats, and the possible protective role of hesperidin (HSD). Oral administration of ALP at 1.15 mg/kg body weight (1/10 LD50) for 30 days resulted in a significant increase in testicular malondialdehyde, lipid hydroperoxides, and oxidized protein levels. These indicators of oxidative stress were accompanied by decreased activity of the antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase, followed by a drastic reduction in the non-enzymatic antioxidant indices of glutathione and total antioxidant capacity when compared to control. Furthermore, ALP treatment produced a marked reduction in sperm count, motility and viability while increasing abnormal sperm morphology and adverse histopathological changes in testis. Co-administration with HSD significantly ameliorated ALP-induced testicular damage by suppressing oxidative stress indices and enhancing antioxidant status while also improving the sperm parameters and histological alterations in ALP-treated rats. The results of the present study indicated that testicular toxic effects of ALP are due to oxidative imbalance and that HSD could be a potential therapeutic agent against ALP-induced testicular damage.

The aim of this study was to establish the effects of fl uoride on lipid metabolism and attendant infl ammatory response by exposing rats to 50 mg L -1 and 100 mg L -1 of fl uoride through drinking water for seven weeks. Both concentrations led to hypercholesterolemia while the 100 mg L -1 concentration induced hypertriglyceridaemia. High density lipoprotein (HDL) cholesterol levels dropped in the exposed rats while interleukin 2 (IL-2) increased more than 1.5-fold (p<0.05) and IL-6 and plasma TNF-α more than 2.5 fold (p<0.05). Fluoride-exposed rats also had signifi cantly higher levels of liver malondialdehyde (MDA) and plasma lipid hydroperoxide (LOOH) but lower plasma paraoxonase (PON1) activity. Oxidative stress indices correlated with pro-infl ammatory cytokines and plasma cholesterol. In contrast, proinfl ammatory cytokines inversely correlated with plasma triglyceride, HDL cholesterol and PON1. Our results suggest that the association between fl uoride exposure with cardiovascular diseases may be related to its ability to disturb lipid homeostasis, and trigger pro-infl ammatory cytokines and oxidative stress.