Abstract

Chlorpyrifos (CPF), a widely used organophosphate pesticide, is reported to severely impair mammalian reproductive system. Pterostilbene (PTS), an effective free radical scavenger, is considered as beneficial for mammalian reproduction. However, the toxicity of CPF on oocyte maturation and whether PTS can eliminate the detrimental effect of CPF on oocytes remain unclear. Here, porcine oocytes were applied to investigate the potential effect and possible mechanism of CPF and PTS during oocyte maturation. This work demonstrated that CPF significantly delayed the meiotic progression and decreased the polar body extrusion by disturbing spindle assembly and chromosome alignment and causing DNA damage in oocytes (p < 0.05). And, CPF significantly impaired oocyte cytoplasmic maturation by inducing the high level of reactive oxygen species and decreasing glutathione content (p < 0.05). Moreover, CPF significantly triggered embryo apoptosis and reduced the blastocyst rate and cell number following parthenogenetic activation (p < 0.05). Whereas CPF-exposed oocytes were treated with PTS, these defects caused by CPF were obviously rescued, and oocyte maturation and subsequent embryonic development were also significantly ameliorated (p < 0.05). In conclusion, these results revealed that CPF exerted the toxic effect on porcine oocytes, while PTS effectively alleviated CPF-induced damage on oocytes. This work provides a potential strategy to protect oocyte maturation in mammalian species.

Highlights

  • Reproductive toxicity is considered as a most common pathological cause of mammalian infertility (Mourikes and Flaws, 2021)

  • Previous studies have suggested that the toxicity induced by CPF could be associated with the induction of reactive oxygen species (ROS) and the broken of antioxidant-prooxidant balance, and the over production of free radicals due to CPF exposure has been shown to cause the oxidation of thiol groups of glutathione (GSH) which is defined as the intracellular redox buffer and protects cells against oxidative stress, increase DNA damage, disturb cell cycle, and result in cell apoptosis or death (Li et al, 2015; Chen et al, 2018; Salyha and Salyha, 2018)

  • The results displayed that when oocytes were treated with the various concentration CPF, 0.25, 0.50 or 1.00 μM CPF significantly decreased the rate of oocyte maturation, and increased the percentage of oocyte death compared with the CON group (Supplementary Table S2, p < 0.05)

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Summary

Introduction

Reproductive toxicity is considered as a most common pathological cause of mammalian infertility (Mourikes and Flaws, 2021). CPF, a conventional broad-spectrum chlorinated OP insecticide, is widely used to control pests to enhance agricultural production, continuous CPF exposure is detrimental to mammalian health due to the cumulatively toxic effect (Ubaid Ur Rahman et al, 2021). Previous studies have suggested that the toxicity induced by CPF could be associated with the induction of reactive oxygen species (ROS) and the broken of antioxidant-prooxidant balance, and the over production of free radicals due to CPF exposure has been shown to cause the oxidation of thiol groups of glutathione (GSH) which is defined as the intracellular redox buffer and protects cells against oxidative stress, increase DNA damage, disturb cell cycle, and result in cell apoptosis or death (Li et al, 2015; Chen et al, 2018; Salyha and Salyha, 2018). These available reports suggest that CPF exposure could disrupt female reproduction

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