Graphical Infertility affects millions of couples worldwide. Oxidative stress (OS) causes peroxidation of lipids and damage to spermatozoa, thus, reducing the quality of seminal parameters. In addition, the differences in the levels of antioxidants and reactive oxygen species (ROS) caused by intrinsic and extrinsic variables linked to lifestyle, diet, genetics, and OS also contribute to male infertility. High levels of ROS result in sperm damage of sperm parameters due to lipid peroxidation and oxidation of proteins. Other significant causes of ROS include changes in sex hormone levels, sperm DNA damage, including mutations, and immature spermatozoa. Treating the root causes of OS, by changing one’s lifestyle, as well as antioxidant therapy, may be helpful strategies to fight OS-related infertility. However, the determination of male infertility induced by OS is currently a challenge in the field of reproductive health research. This review intends to describe the role of oxidative stress on male infertility and the current understanding of its management. Lay summary: The inability to conceive affects many couples globally. Oxidative stress refers to imbalances between different oxygen species which can lead to male fertility problems by damaging sperm and semen. Oxidative stress may be caused by several factors, including diets high in fats, sugars and processed foods, lifestyle (including smoking, alcohol consumption and having a sedentary lifestyle), and genetics. Treatment that focuses on the root cause may help combat male infertility. However, there is currently no consensus on the best way to treat male fertility problems, particularly those associated with oxidative stress. This paper describes the role of oxidative stress on male infertility and discusses the current techniques employed in treating male fertility issues.

Leydig cells are essential for steroidogenesis and spermatogenesis. An imbalance in the production of reactive oxygen species (ROS) and the cellular antioxidant level brings about oxidative stress. Oxidative stress (OS) results in the dysfunction of Leydig cells, thereby impairing steroidogenesis, spermatogenesis, and ultimately, male infertility. To prevent Leydig cells from oxidative insults, there needs to be a balance between the ROS production and the cellular protective capacity of antioxidants. Evidence indicates that medicinal plants could improve Leydig cell function at specific concentrations under basal or OS conditions. The increased usage of medicinal plants has been considered a possible alternative treatment for male infertility. This review aims to provide an overview of the impact of oxidative stress on Leydig cells as well as the effects of various medicinal plant extracts on TM3 Leydig cells. The medicinal plants of interest include Aspalathus linearis, Camellia sinensis, Moringa oleifera, Morinda officinale, Taraxacum officinale, Trichilia emetica, Terminalia sambesiaca, Peltophorum africanum, Ximenia caffra, Serenoa repens, Zingiber officinale, Eugenia jambolana, and a combination of dandelion and fermented rooibos (CRS-10). According to the findings obtained from studies conducted on the evaluated medicinal plants, it can, therefore, be concluded that the medicinal plants maintain the antioxidant profile of Leydig cells under basal conditions and have protective or restorative effects following exposure to oxidative stress. The available data suggest that the protective role exhibited by the evaluated plants may be attributed to their antioxidant content. Additionally, the use of the optimal dosage or concentration of the extracts in the management of oxidative stress is of the utmost importance, and the measurement of their oxidation reduction potential is recommended.

According to a recent report by the WHO, 50–80 million people suffer with infertility. Amongst these populations, male counterparts account for 20–50% of infertility cases. The aetiology of infertility in men includes many factors such as psychological issues, lifestyle and environmental factors, hormonal disorders and chromosomal abnormalities. The pathophysiology of these aetiologies may be initiated by a local inflammatory reaction increasing reactive oxygen species (ROS) production, which can negatively affect the male reproductive system by altering the hypothalamic–pituitary–gonadotropin axis (HPG axis). Alteration of the HPG axis may affect testicular steroidogenesis, spermatogenesis, the Leydig cells and Sertoli cells, leading to poor semen quality. The prevalence of male infertility underscores the need for a thorough scientific investigation to identify treatable or reversible factors using plant adjuvants with antioxidative properties. Therefore, this review aims to provide an overview of the currently available knowledge on the aetiologies of male reproductive dysfunction, emphasising infertility risk factors, as well as elucidating the possible ways by which readily available alternatives, such as Moringa oleifera leaves, may mitigate male infertility by highlighting its role on the oxidative stress parameters, reproductive hormonal levels, testicular steroidogenesis and spermatogenesis, gene expression, weight and morphology of the testis and sperm parameters.

Green tea is a popularly consumed beverage worldwide and contains polyphenols, whose antioxidant activities could improve sperm parameters and fertility thereof. We investigated the effect of green tea on the male rat reproductive system as well as its safety. Male Wistar rats were administered 2 and 5% aqueous extract of green tea for 52 days’ ad libitum, while the control group received tap water. Total polyphenol, flavanol, flavonol and soluble solids significantly increased in a concentration-dependent manner in vitro (P < 0.01). Weights of body, testis, epididymis, prostate gland, seminal vesicles, and liver, serum levels of testosterone, ferric reducing antioxidant power, creatinine, and sperm motility, remained unchanged (P > 0.05). Kidney weight, sperm concentration and vitality, spontaneous acrosome reaction increased (P < 0.05), while alanine transaminase and aspartate transaminase levels decreased (P< 0.05). Catalase, superoxide dismutase, glutathione and lipid peroxidation remained unchanged in the testes, liver and kidney (P > 0.05). Histological sections of testis, epididymis, kidney and liver showed no conspicuous alteration. Diameter and epithelial height of seminiferous tubule decreased, while caudal epididymis epithelial height increased (P < 0.01). Consumption of green tea in the conditions used in the present study seems to be safe and improved sperm parameters. However, subtle structural changes observed in the decreased diameter and epithelial height of the seminiferous tubule and increased acrosome reaction needs further investigation.

Diabetes mellitus (DM) significantly impairs male reproductive health, largely through hyperglycemia‐induced oxidative stress (OS). Elevated glucose activates detrimental metabolic pathways, notably the polyol pathway, which depletes antioxidant defenses and generates reactive oxygen species (ROS). This oxidative burden damages spermatozoa, leading to reduced motility, abnormal morphology, DNA fragmentation, and disrupted membrane integrity. OS also compromises the hypothalamic–pituitary–gonadal axis, lowering testosterone synthesis and impairing spermatogenesis. The formation of advanced glycation end products (AGEs) and chronic inflammation further exacerbate Leydig and Sertoli cell dysfunction, microvascular injury, and testicular apoptosis. Clinical evidence consistently links DM to deteriorated semen parameters, hormonal imbalances, and reduced natural conception rates, with poorer outcomes in assisted reproductive technologies. Obesity and metabolic syndrome, common comorbidities in DM, amplify oxidative stress and further impair fertility potential. While seminal plasma contains enzymatic and non‐enzymatic antioxidants, these defenses are often insufficient in diabetic men. Targeted interventions, including antioxidant therapy, lifestyle modifications, glycemic control, and management of comorbidities, offer promise in mitigating oxidative damage. This review synthesizes current evidence on the molecular, endocrine, and clinical consequences of DM‐related oxidative stress on male fertility, underscoring the need for integrated management strategies to preserve reproductive function in diabetic men.