The male factor is considered a major contributory factor to infertility. Apart from the conventional causes for male infertility such as varicocoele, cryptorchidism, infections, obstructive lesions, cystic fibrosis, trauma and tumours, a new and important cause has been identified as being responsible for the so-called idiopathic male infertility: oxidative stress. Oxidative Stress (OS) is a condition that occurs when the production of Reactive Oxygen Species (ROS) overwhelms the antioxidant defense produced against them. In male reproductive pathological conditions, the OS significantly impairs spermatogenesis and sperm function, which may lead to male infertility. Reactive Oxygen Species (ROS) known as free radicals are oxidizing agents generated as a result of metabolism of oxygen and have at least one unpaired electron that make them very reactive species. Spermatozoa generate Reactive Oxygen Species (ROS) in physiological amounts, which play a role in sperm functions during sperm capacitation, Acrosome Reaction (AR) and oocyte fusion, but they need to be controlled and their concentrations maintained at a level that is not deleterious to the cells. Administration of antioxidants in patients with 'male factor' infertility has begun to attract considerable interest. The main difficulty of such an approach is our incomplete understanding of the role of free radicals in normal and abnormal sperm function leading to male infertility. The purpose of the present review is to address the relationship between ROS and idiopathic male factor infertility.

In the last 50 years the incidence of infertility, testicular and prostate cancers and associated maladies has increased significantly. Infertility now affects 15-20% of couples as opposed to 7-8% fifty years ago. Average sperm counts among adult men have decreased by 50% since 1938, with a decline of 2% every year from 1973. This decline in male reproductive health has been linked to an increased presence in the environment of chemical contaminants in the form of pesticides and plastics. Rapid and unplanned industrialization caused large amounts of these synthetic compounds and their by-products to be released in the environment (air, soil, water and food). Studies have shown that occupational exposure to pesticides caused neonatal deaths, congenital defects, testicular dysfunction and male infertility. Many of these chemicals found in our environment and households have oestrogenic properties ("xenoestrogens") and are toxic because they affect the endocrine system ("endocrine disruptors"). Evidence of the health hazards of endocrine disrupting chemicals continues to mount. In terms of male fertility, it now seems that these ubiquitous chemicals are a significant threat at various stages, from testicular development to sperm production to the functionality of healthy sperm. This class of chemicals appears to be threatening male fertility on several fronts. That endocrine disruptors abound in our environment is not in doubt. Clinicians and other health practitioners confronted with the challenges of managing male infertility should attempt to identify the aetiology of a possible exposure to endocrine disruptors, and initiate a plan to control and prevent exposure to others. In addition, concerted efforts should be made by both government and non-governmental agencies to institute local studies that will assess local endocrine disruptors, degree of contamination, level of exposure and proffer control and preventive measures. Emphasis should be placed on establishment of chemical screening and testing program, research into dose and vulnerable periods, institution of surveillance of disease incidence, improvement of exposure monitoring, and educating community leaders and the public in general.

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Phenytoin, an antiepileptic drug is used in managing seizures. Phenytoin-associated oxidative stress causes cellular damage by the generation of free radicals. Vitamin C, a standard antioxidant and Calotropis procera are believed to scavenge oxygen free radicals. The effect of C. procera extract on haematological and biochemical variables in an in-vivo model was studied. Pregnant rats were administered phenytoin (50 mg/kg body weight). Extracts of C. procera (300 mg/kg body weight) and vitamin C (200 mg/kg body weight) were administered one hour prior to phenytoin treatment separately, while control animals received tap water only. The animals had access to food and water ad libitum. Blood was collected from animals on day 50 postpartum for packed cell volume (PCV), haemoglobin (Hb) content and evaluation of levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) evaluation. Lipid peroxidase (LPO) and reduced glutathione (GSH) levels in the cerebellum were assessed as markers of oxidative stress on day 50 postpartum. Phenytoininduced toxicity was associated with increased cerebellar LPO and decreased GSH levels. Increase in ALT and AST levels in the serum was observed. However, PCV and Hb levels were not affected. LPO, GSH, ALT and AST levels registered a tendency to shift towards normalcy on administration of C. procera and vitamin C to phenytoin. In conclusion, supplementation with C. procera leaf extract reduced the rate at which phenytoin induced toxicity in developing rat cerebellum postnatally.