Pyrethroids Toxicity to Male Reproductive System and Offspring as a Function of Oxidative Stress Induction: Rodent Studies

Abstract

Pyrethroids may be related to male reproductive system damage. However, the results of many previous studies are contradictory and uncertain. Therefore, a systematic review and a meta-analysis were performed to assess the relationship between pyrethroid exposure and male reproductive system damage. A total of 72 articles were identified, among which 57 were selected for meta-analysis, and 15 were selected for qualitative analysis. Pyrethroid exposure affected sperm count (SMD= -2.0424; 95% CI, -2.4699 to -1.6149), sperm motility (SMD=-3.606; 95% CI, -4.5172 to -2.6948), sperm morphology (SMD=2.686; 95% CI, 1.9744 to 3.3976), testis weight (SMD=-1.1591; 95% CI, -1.6145 to -0.7038), epididymal weight (SMD=-1.1576; 95% CI, -1.7455 to -0.5697), and serum testosterone level (SMD=-1.9194; 95% CI, -2.4589 to -1.3798) in the studies of rats. We found that gestational and lactational exposure to pyrethroids can reduce sperm count (SMD=1.8469; 95% CI, -2.9010 to -0.7927), sperm motility (SMD=-2.7151; 95% CI, -3.9574 to -1.4728), testis weight (SMD=-1.4361; 95% CI, -1.8873 to -0.9848), and epididymal weight (SMD=-0.6639; 95% CI, -0.9544 to -0.3733) of F1 offspring. Exposure to pyrethroids can increase malondialdehyde (SMD=3.3451; 95% CI 1.9914 to 4.6988) oxide in testes and can reduce the activities of glutathione (SMD=-2.075; 95% CI -3.0651 to -1.0848), superoxide dismutase (SMD=-2.4856; 95% CI -3.9612 to -1.0100), and catalase (SMD=-2.7564; 95% CI -3.9788 to -1.5340). Pyrethroid exposure and oxidative stress could damage male sperm quality. Gestational and lactational pyrethroid exposure affects the reproductive system of F1 offspring.

Mitigating properties of vitamin E and olive oil on the teratomorphogenic impacts of lambda-cyhalothrin in developing chick embryos

“…These findings were in line with most of the studies which suggested that LCH exposure causes depletion of proteins by causing the destruction or necrosis of cellular function and consequent impairment in protein synthetic machinery [8] , [13] , [18] , [33] . As most of the pyrethroids inflict intense oxidative stress even in the adult tissues and organs [3] , [36] , it is proposed that LCH exposure in present study must have led to an intense increase in the reactive oxygen radicals in the developing embryos as the metabolic rate of the differentiating tissues and organs is naturally much higher than the adult tissues and are more prone to oxidative damage. Additionally, the embryonic tissues are less differentiated and are thus metabolically insufficient to metabolize the insecticide and to get rid of its metabolites and also to combat with the reactive oxygen species generated on insecticide exposure [21] , [24] .…”

Identification of Glucose Metabolism-Related Genes in the Progression from Nonalcoholic Fatty Liver Disease to Hepatocellular Carcinoma

“…However, there are also some limitations to bioinformatics analysis. First, without experimental verification, the results need to be verified by experiments [ 40 ]. In addition, high heterogeneity often leads to large bioinformatics analysis errors, so unifying the methods is essential to reducing errors [ 41 ].…”

Update on mosquito bite reaction: Itch and hypersensitivity, pathophysiology, prevention, and treatment

“…Permethrin is a broadly used, long-lasting pyrethroid insecticide coated on fabrics and mosquito nets, particularly in malaria-endemic countries enforcing control programs to curtail disease transmission. Permethrin also has some toxicity concerns, including a reduction in male fertility parameters and reduced testosterone demonstrated in rodent studies ( 65 ) as well as hepatotoxicity ( 66 ). The widespread use of pyrethroid insecticides has gained exponential traction over the past few years as mosquitos have developed pyrethroid resistance.…”