Trans‐ovo permethrin exposure affects growth, brain morphology and cardiac development in quail

Abstract

Permethrin is a commonly used, highly effective pesticide in poultry agriculture, and has recently been trialed in conservation efforts to protect Galápagos finch hatchlings from an invasive ectoparasite. Although permethrin is considered safe for adults, pesticides can have health consequences when animals are exposed during early life stages. The few studies that have examined permethrin's effects in embryonic chicks and rats have shown hydrocephaly, anencephaly, reduced cellular energy conversion, and disruption of developing heart muscle. To test whether trans‐ovo exposure of permethrin affects early development in birds, we exposed Japanese quail (Coturnix japonica) eggs to cotton treated with 1% permethrin that was incorporated into nests in two amounts (0.2, 0.8 g), each with a paired untreated cotton control group. When measured on incubation Day 15, we found permethrin‐treated developing birds were smaller and showed signs of microcephaly, although mortality rates were the same. Despite no difference in heart mass, ventricular tissue was less compact, cardiac arteries were reduced and heart rates were slower in permethrin‐treated birds. Differences in heart development were also observed at 5 days of incubation, indicating that abnormalities are present from early in cardiac development. Future studies are needed to examine permethrin's effects on developmental pathways and to determine if these effects persist after hatching to affect offspring health. This study provides evidence that permethrin can cross the eggshell to cause non‐lethal but adverse effects on embryonic development, and studies should look beyond hatching when monitoring the efficacy of permethrin on wild bird populations.

Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

“…[72][73][74] Furthermore, there were only a few studies about the exposure of pyrethroid induced the change of brain morphology. 75,76 According to report, in mouse cells, DLM can continuously increase the content of Ca 2+ in cells, and the imbalance of Ca 2+ homeostasis will promote ER stress. 77 The response of ER stress will produce a large amount of CHOP, which inhibits the expression of Bcl-2 located on the mitochondrial membrane, thereby promoting apoptosis of the mitochondrial pathway.…”

“…Studies on the effects of DLM neurotoxic have been reported in mammals, fish, and insects 72–74 . Furthermore, there were only a few studies about the exposure of pyrethroid induced the change of brain morphology 75,76 . According to report, in mouse cells, DLM can continuously increase the content of Ca 2+ in cells, and the imbalance of Ca 2+ homeostasis will promote ER stress 77 .…”

Protective effects of resveratrol on permethrin-induced fetotoxicity in rats

“…Perm, due to its lipophilic properties, accumulates in tissues with high lipid content such as liver, kidney and breast, as well as fat and nervous system, and is metabolized in the liver and excreted through the kidneys (Ding et al, 2013). Experimental studies have shown that Perm adversely affects the peripheral and central nervous system in mammals, causes neurotoxic effects by inducing oxidative stress in the neonatal rat brain, increases malondialdehyde levels by causing lipid peroxidation, has advers effects on the liver and endocrine system, and causes degenerative and necrotic damage in the kidney, increases apoptotic cell death, decreases sperm concentration in rats, and causes heart diseases (Wang et al, 2016;Romero et al, 2017;Curtis et al, 2021). These undesirable effects of Perm can cause fetal toxicity and developmental delay in offspring, especially during pregnancy.…”

A mixture of pyrethroids induces reduced fecundity and increased testicular genotoxicity in rats

“…We presented an extensive review on the toxic effects of pyrethroids at multiple levels (Ravula & Yenugu, 2021c). Recent studies report that bifenthrin causes reduction in pregnancy potential and defects in fetal growth and development (Curtis et al, 2021; Park et al, 2021). Malformation of male gamates, DNA damage and epimutations in sperm and reproductive toxicity were evident in animal models that were exposed to fenvalerate, cypermethrin, permethrin, deltamethrin and fenpropathrin, respectively (Abu Zeid et al, 2021; Ha et al, 2021; Hozyen et al, 2020; Huang et al, 2021; Thorson et al, 2020).…”