Advancements in Genetic Biomarkers and Exogenous Antioxidant Supplementation for Safeguarding Mammalian Cells against Heat-Induced Oxidative Stress and Apoptosis

Abstract

Heat stress represents a pervasive global concern with far-reaching implications for the reproductive efficiency of both animal and human populations. An extensive body of published research on heat stress effects utilizes controlled experimental environments to expose cells and tissues to heat stress and its disruptive influence on the physiological aspects of reproductive phenotypic traits, encompassing parameters such as sperm quality, sperm motility, viability, and overall competence. Beyond these immediate effects, heat stress has been linked to embryo losses, compromised oocyte development, and even infertility across diverse species. One of the primary mechanisms underlying these adverse reproductive outcomes is the elevation of reactive oxygen species (ROS) levels precipitating oxidative stress and apoptosis within mammalian reproductive cells. Oxidative stress and apoptosis are recognized as pivotal biological factors through which heat stress exerts its disruptive impact on both male and female reproductive cells. In a concerted effort to mitigate the detrimental consequences of heat stress, supplementation with antioxidants, both in natural and synthetic forms, has been explored as a potential intervention strategy. Furthermore, reproductive cells possess inherent self-protective mechanisms that come into play during episodes of heat stress, aiding in their survival. This comprehensive review delves into the multifaceted effects of heat stress on reproductive phenotypic traits and elucidates the intricate molecular mechanisms underpinning oxidative stress and apoptosis in reproductive cells, which compromise their normal function. Additionally, we provide a succinct overview of potential antioxidant interventions and highlight the genetic biomarkers within reproductive cells that possess self-protective capabilities, collectively offering promising avenues for ameliorating the negative impact of heat stress by restraining apoptosis and oxidative stress.

Bioactive Compounds Protect Mammalian Reproductive Cells from Xenobiotics and Heat Stress-Induced Oxidative Distress via Nrf2 Signaling Activation: A Narrative Review

“…External environmental stressors such as high temperatures and exposure to xenobiotics significantly contribute to the initiation of oxidative stress and apoptosis processes, which have a negative impact on the functionality of reproductive cells [1][2][3][4]. Normally, an organism's intrinsic antioxidant mechanisms are able to counteract the harmful effects of reactive oxygen species (ROS) overproduction, thus maintaining cellular integrity [5].…”

“…To mitigate these effects, the use of external antioxidants is recommended to improve cellular antioxidant capacity and influence important biochemical pathways, including the activation of the Antioxidants 2024, 13, 597 2 of 34 nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. This intervention aims to protect mammalian reproductive cells from oxidative damage and apoptosis [2,[7][8][9].…”

“…Under normal conditions, Nrf2 predominantly resides in the cytoplasm, forming a complex with its inhibitory partner, Kelch-like ECH-associated protein 1 (Keap1). However, in the presence of elevated levels of ROS, this complex dissociates, allowing Nrf2 to translocate from the cytoplasm into the nucleus [2,15,16]. Once activated, Nrf2 binds to the antioxidant response element (ARE) sequence, starting the transcription of genes involved in antioxidant defenses to counteract ROS-induced damage [9,[17][18][19].…”