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Humans and wildlife, including domesticated animals, are exposed to a myriad of environmental contaminants that are derived from various human activities, including agricultural, household, cosmetic, pharmaceutical, and industrial products. Excessive exposure to pesticides, heavy metals, and phthalates consequently causes the overproduction of reactive oxygen species. The equilibrium between reactive oxygen species and the antioxidant system is preserved to maintain cellular redox homeostasis. Mitochondria play a key role in cellular function and cell survival. Mitochondria are vulnerable to damage that can be provoked by environmental exposures. Once the mitochondrial metabolism is damaged, it interferes with energy metabolism and eventually causes the overproduction of free radicals. Furthermore, it also perceives inflammation signals to generate an inflammatory response, which is involved in pathophysiological mechanisms. A depleted antioxidant system provokes oxidative stress that triggers inflammation and regulates epigenetic function and apoptotic events. Apart from that, these chemicals influence steroidogenesis, deteriorate sperm quality, and damage male reproductive organs. It is strongly believed that redox signaling molecules are the key regulators that mediate reproductive toxicity. This review article aims to spotlight the redox toxicology of environmental chemicals on male reproduction function and its fertility prognosis. Furthermore, we shed light on the influence of redox signaling and metabolism in modulating the response of environmental toxins to reproductive function. Additionally, we emphasize the supporting evidence from diverse cellular and animal studies.

Male infertility is a widely debated issue that affects males globally. There are several mechanisms involved. Oxidative stress is accepted to be the main contributing factor, with sperm quality and quantity affected by the overproduction of free radicals. Excess reactive oxygen species (ROS) cannot be controlled by the antioxidant system and, thus, potentially impact male fertility and hamper sperm quality parameters. Mitochondria are the driving force of sperm motility; irregularities in their function may lead to apoptosis, alterations to signaling pathway function, and, ultimately, compromised fertility. Moreover, it has been observed that the prevalence of inflammation may arrest sperm function and the production of cytokines triggered by the overproduction of ROS. Further, oxidative stress interacts with seminal plasma proteomes that influence male fertility. Enhanced ROS production disturbs the cellular constituents, particularly DNA, and sperms are unable to impregnate the ovum. Here, we review the latest information to better understand the relationship between oxidative stress and male infertility, the role of mitochondria, the cellular response, inflammation and fertility, and the interaction of seminal plasma proteomes with oxidative stress, as well as highlight the influence of oxidative stress on hormones; collectively, all of these factors are assumed to be important for the regulation of male infertility. This article may help improve our understanding of male infertility and the strategies to prevent it.

The fetal-maternal immune system determines the fate of pregnancy. The trophoblast cells not only give an active response against external stimuli but are also involved in secreting most of the cytokines. These cells have an essential function in fetal acceptance or fetal rejection. Other immune cells also play a pivotal role in carrying out a successful pregnancy. The disruption in this mechanism may lead to harmful effects on pregnancy. The placenta serves as an immune barrier in fetus protection against invading pathogens. Once the infections prevail, they may localize in placental and fetal tissues, and the presence of inflammation due to cytokines may have detrimental effects on pregnancy. Moreover, some pathogens are responsible for congenital fetal anomalies and affect almost all organs of the developing fetus. This review article is designed to address the bacterial and viral infections that threaten pregnancy and their possible outcomes. Moreover, training of the fetal immune system against the exposure of infections and the role of CD49a + NK cells in embryonic development will also be highlighted.

Antibiotic-resistant bacteria causing foodborne serious illnesses can be found in contaminated food. Therefore, this study aimed to identify the pathogens, genes, and antimicrobial residues present in raw milk and meat. We collected 40 raw milk and 40 beef samples using the aseptic method from various parts of the Faisalabad metropolis, Pakistan. The samples were cultured on blood, MacConkey, and UTI chrome agar. The VITEK 2 compact system was used for microbial identification and determination of minimum inhibitory concentrations. Antimicrobial resistance genes for extended-spectrum β-lactamases, methicillin resistance in Staphylococcus aureus, and carbapenem resistance were identified using molecular techniques. ELISA was used to determine the tetracycline residue level in each sample. The beef samples showed polymicrobial contamination with 64 bacterial isolates, with Escherichia coli (29; 45.3%) and Klebsiella pneumoniae (11; 17.1%) predominating. The milk samples showed polymicrobial contamination with 73 bacterial isolates, with E. coli (22; 30%), K. pneumoniae (12; 16.4%), and S. aureus (10; 13.6%) forming the majority. Twenty-eight (43.7%) isolates from beef harbored tet genes, nineteen (29.6%) blaCTX-M, and fourteen (21.8%) blaNDM-1, and twenty-six (35.6%) isolates from milk harbored tet genes, nineteen (26%) blaTEM and blaCTX-M, and three (4%) blaNDM-1. Twenty-two (55%) each of the beef and milk samples exceeded the maximum residue limit for tetracycline. Polymicrobial contamination by bacteria possessing blaCTX-M, blaTEM, blaNDM-1, blaOXA, mecA, and tet genes was identified in food samples. The high tetracycline residue levels pose a serious health risk to consumers.

It has been widely known that oxidative stress disrupts the balance between reactive oxygen species (ROS) and the antioxidant system in the body. During pregnancy, the physiological generation of ROS is involved in a variety of developmental processes ranging from oocyte maturation to luteolysis and embryo implantation. While abnormal overproduction of ROS disrupts these processes resulting in reproductive failure. In addition, excessive oxidative stress impairs maternal and placental functions and eventually results in fetal loss, IUGR, and gestational diabetes mellitus. Although some oxidative stress is inevitable during pregnancy, a balancing act between oxidant and antioxidant production is necessary at different stages of the pregnancy. The review aims to highlight the importance of maintaining oxidative and antioxidant balance throughout pregnancy. Furthermore, we highlight the role of oxidative stress in pregnancy-related diseases.

Defective implantation is related to pregnancy-associated disorders such as spontaneous miscarriage, intrauterine fetal growth restriction and others. Several factors proclaimed to be involved such as physiological, nutritional, environmental and managemental that leads to cause oxidative stress. Overloading of free radicals promotes oxidative stress, and the internal body system could not combat its ability to encounter the damaging effects and subsequently leading to pregnancy-related disorders. During pregnancy, essential amino acids display important role for optimum fetal growth and other necessary functions for continuing fruitful pregnancy. In this context, dietary amino acids have received much attention regarding the nutritional concerns during pregnancy. Arginine, glutamine, tryptophan and taurine play a crucial role in fetal growth, development and survival while ornithine and proline are important players for the regulation of gene expression, protein synthesis and angiogenesis. Moreover, amino acids also stimulate the mammalian target of rapamycin (mTOR) signaling pathway which plays a central role in the synthesis of proteins in placenta, uterus and fetus. This review article explores the significances of dietary amino acids in pregnancy development, regulation of nutrient-sensing pathways such as mTOR, peroxisome proliferator-activated receptors (PPARs), insulin/insulin-like growth factor signaling pathway (IIS) and 5′ adenosine monophosphate-activated protein kinase (AMPK) which exhibit important role in reproduction and its related problems. In addition, the antioxidant function of dietary amino acids against oxidative stress triggering pregnancy disorders and their possible outcomes will also be enlightened. Dietary supplementation of amino acids during pregnancy could help mitigate reproductive disorders and thereby improving fertility in animals as well as humans.