Mechanisms of female reproductive toxicity in pigs induced by exposure to environmental pollutants.

Environmental pollutants, including endocrine disruptors, heavy metals, nanomaterials, and pesticides, have been detected in various ecosystems and are of growing global concern. The potential for toxicity to non-target organisms has consistently been raised and is being studied using various animal models. In this review, we focus on pesticides frequently detected in the environment and investigate their potential exposure to livestock. Owing to the reproductive similarities between humans and pigs, various in vitro porcine models such as porcine oocytes, trophectoderm cells, and luminal epithelial cells, are used to verify the reproductive toxicity. These cell lines are being used to study the toxic mechanisms induced by various environmental toxicants, including organophosphate insecticides, pyrethroid insecticides, dinitroaniline herbicides, and diphenyl ether herbicides, which persist in the environment and threaten livestock health. Collectively, these results indicate that these pesticides can induce female reproductive toxicity in pigs and suggest the possibility of adverse effects on other livestock species. These results also indicate possible reproductive toxicity in humans, which requires further investigation.

Pyridaben induces apoptosis and inflammation in bovine mammary epithelial cells by disturbance of calcium homeostasis and upregulation of MAPK cascades.

Pyridaben is a widely used pyridazinone insecticide used to protect crops against insects and mites. The toxicity of pyridaben has been reported in mice, zebrafish, the human reproductive system, nervous system, and respiratory system. Pyridaben can also be ingested by dairy cattle through feed. However, the toxicity of pyridaben in cattle has not been investigated on. Thus, this study focuses on demonstrating the toxicity of pyridaben in the bovine mammary glands and with the generation milk in the bovine mammary epithelial cells, as it is crucial to the continuance of the amount and the quality of the milk produced. We started by analyzing the intracellular toxicity along with the impact of pyridaben on the cell cycle distribution and the transcription of associated genes. Pyridaben treatment induced cell cycle arrest accompanied the disruption in G1 and S phases with imbalanced cytosolic and mitochondrial calcium ion homeostasis, and caused a destruction of mitochondrial membrane potential. This eventually led to apoptosis of MAC-T cells. We also investigated in the impact that pyridaben has on MAPK signaling proteins, where phosphorylation of ERK1/2, JNK, and p38 were upregulateed. Moreover, examination of the effect of pyridaben in the inflammatory genes revealed hyperactivation of the inflammatory gene transcription. This is the first research to assess the negative outcomes that pyridaben could impose on dairy cattle and milk production.