Oxidative stress and inflammation following sub-lethal oral exposure of cypermethrin in rats: mitigating potential of epicatechin

• Main Authors: Olusegun Kayode Afolabi, Felix Adesola Aderibigbe, Dasola Teslim Folarin, Abimbola Arinola, Adedoja Dorcas Wusu
• Format: Article
• Language: English
• Published: Elsevier 2019-08-01
• Series: Heliyon
• Subjects: Food science; Environmental hazard; Environmental toxicology; Biochemistry; Toxicology; Cypermethrin
• Online Access: http://www.sciencedirect.com/science/article/pii/S2405844019359341

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−1 body weight), CYP (25 mg kg−1 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 CYP-exposed rats mitigated the induced oxidative and inflammatory effects. These data suggest that EC can attenuate the toxic effects induced by CYP exposure.