review · Frontiers in Endocrinology
Oxidative stress is a primary factor contributing to male infertility worldwide, directly reducing both the quality and quantity of sperm. When the body antioxidant defences are overwhelmed by an excess of reactive oxygen species, cellular components suffer damage. In particular, sperm DNA is harmed, which prevents successful fertilisation of an ovum. Crucial cell structures such as mitochondria, which generate the energy required for sperm motility, also experience dysfunction under oxidative stress, triggering cell death and disrupting cellular signalling pathways. Furthermore, excess reactive oxygen species trigger inflammatory responses and cytokine production that disrupt normal sperm activity. Oxidative stress also alters seminal plasma proteins and interferes with hormonal regulation, reinforcing its multifaceted impact on reproductive health and highlighting the importance of developing protective strategies.
Male infertility affects millions of couples globally, yet the underlying biological causes often remain difficult to diagnose and manage. Understanding how oxidative stress damages sperm structures, alters cellular proteins, and triggers inflammation helps clarify why fertility declines. These insights provide a scientific foundation for identifying risk factors and guiding lifestyle or medical interventions aimed at preserving reproductive health.
This work represents early-stage, mechanistic research reviewing biological pathways rather than testing a specific product. The detailed insights into reactive oxygen species, mitochondrial impairment, and seminal proteomes could ultimately guide reproductive health companies and clinical researchers developing diagnostic assays or targeted antioxidant interventions. However, practical preventive strategies or therapeutic applications remain at a conceptual stage and require dedicated formulation and clinical testing.
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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.
This page summarises published work. The authoritative version sits with the publisher.
DOI: 10.3389/fendo.2023.1070692
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