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.

This study was aimed at evaluating the protective role of catechin (CT) against toxicity induced by combined exposure to arsenic (As) and deltamethrin (DM) in rats. Thirty-five (35) male Wistar rats were divided into 5 groups of 7 animals each. Treatment of each group was as follows: Control (C) administered corn oil (1ml kg -1 ), catechin only (CT) at 40mg kg -1 , As+DM administered As (100ppm) in their drinking water and DM at a dose of 7.5mg kg -1 (1/20 th LD 50 ), As+DM-CT 40 treated as As+DM in addition to oral administration of CT at 40mg kg -1 while the last group, As+DM-CT 80 received the same treatment as As+DM, along with oral CT treatment at a dose of 80mg kg -1 . The treatment lasted for 28 days. Effect of the treatment in inducing oxidative damage was appraised by estimating levels of lipid peroxidation, protein oxidation, glutathione and total antioxidant capacity in the liver, kidney, and testis of the rats. Also, the activities of superoxide dismutase, catalase, and glutathione peroxidase were assayed in the tissues. For the evaluation of inflammation, plasma levels of interleukin-6, tumor necrosis factor-alpha and 8-nitroguanine were determined. The result showed that the combination of As and DM gave rise to marked alterations of these parameters but supplementation with CT attenuated these effects.

Background: Taurine is a conditional essential nutrient in man, with proven antioxidant property. This study was designed to evaluate the protective effects of taurine against atrazine (ATZ)-induced hepatic and renal oxidative toxicity in rats.Methods: Wistar rats were orally exposed to ATZ (1/10 LD50) alone or in combination with taurine at 1.5% w/v and 3% w/v in their drinking water for 30 days. After treatment, the liver and kidney were excised for biochemical assays by spectrophotometric methods.Results: Exposure to ATZ significantly elevated hepatic and renal malondialdehyde (MDA) levels when compared to control (p < 0.05). Advanced oxidized protein products (AOPP) were equally increased in these tissues on exposure to ATZ. In addition, reduced glutathione (GSH) and total antioxidant capacity (TAC) were markedly depleted in both organs on exposure to ATZ. Furthermore, activities of the antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) were inhibited by ATZ compared to the control. However, co-treatment with taurine attenuated the oxidative responses generated by ATZ exposure in the rats, with the high dose of the amino acid normalizing most of the toxic effects.Conclusion: The study suggested that taurine can protect against ATZ-induced oxidative stress.