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

Abstract

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.

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“…When they get saturated GPX is activated that to detoxifies H 2 O 2 . Similar to other studies, oxidative stress is increased with a decreased level of GPX, SOD & CAT activities in group II [21,23] . In PBMC + withdrawal group (Group III) partial recovery of these enzymes was evident in our study.…”

Effect of Lambdacyhalothrin on Locomotor Activity, Memory, Selected Biochemical Parameters, Tumor Necrosis Factor α, and Interleukin 1ß in a Mouse Model

“…There are many reports confirming that exposure on pyrethroids causes oxidative stress and in this mechanism causes an increase in the expression of genes encoding proinflammatory cytokines [ 49 , 50 , 51 , 52 , 53 , 54 , 55 ]. The interleukin1β is primarily synthesized in macrophages and monocytes.…”

Bioallethrin enhances generation of ROS, damages DNA, impairs the redox system and causes mitochondrial dysfunction in human lymphocytes

“…A known and major cause for such cell killing is oxidative stress which, above a threshold, is very damaging, even fatal, to any human/non-human cell 40 , 41 . Several studies have reported that pyrethroids can induce oxidative stress condition leading to cell damage and death 42 – 44 . Well known markers of oxidative stress include monitoring lipid and protein oxidation and levels of glutathione (reduced and oxidised).…”