CREM, PRM I and II gene expression in Wistar rats testes treated with antipsychotic drugs: Chlorpromazine, Rauwolfia vomitoria and co-administration of reserpine, zinc and ascorbic acid.

OBJECTIVE: The literature has shown that synthetic antipsychotic drugs induce reproductive toxicity, while psychiatric patients treated with traditionally used antipsychotic herbs (Rauwolfia vomitoria) showed no traces of reproductive toxicity. Thus, this study aimed to investigate the expression of CREM, PRM I and II genes in the testes of Wistar rats treated with antipsychotic drugs: chlorpromazine, Rauwolfia vomitoria (RV) and co-administration of reserpine, zinc and ascorbate (RAZ). METHODS: Forty-five adult male Wistar rats with rats with average weight of 180±4.67g were divided into nine groups (A-I) (n=5). Group A was administered saline (control) while rats in Groups B and C received 10 and 20mg/kg body weight (bwt) of chlorpromazine respectively. Groups D and E received 2.5 and 5mg/kg bwt of reserpine, respectively; while Groups F and G received 150 and 300mg/kg bwt of RV leaf extract. Groups H and I received (2.5+5+100) mg/kg bwt and (5+10+200) mg/kg of combination of RAZ, respectively for 56 days. RESULTS: The CREM, PRM I and II genes were significantly downregulated while significant decreased in serum FSH and testosterone concentration were found in the Chlorpromazine- and Reserpine-treated groups. Groups H and I showed a highly significant upregulation of the CREM, PRM I and II genes, and a highly significant increase in serum FSH and testosterone concentrations. CONCLUSION: The study concluded that the HPT-Axis was impaired by chlorpromazine and reserpine, while RV and a combination of RAZ administration enhanced the axis in an animal model. The study recommended that synthetic antipsychotic drugs should be taken with Zinc and Ascorbate in order to help prevent reproductive toxicity associated with antipsychotic drugs. We need further studies in humans to confirm these findings.

Review on the role of glutathione on oxidative stress and infertility.

Infertility is a global health problem and it is one of the most stressful conditions amongst married couples. Even though not lethal, it has been described as a radical life changing problem that carries with it significant psychological trauma. Infertility can be caused by various problems and sometimes it is not possible to establish a cause. Oxidative stress, which arises from an imbalance between reactive oxygen species (ROS) and protective antioxidants, influences the entire reproductive lifespan of men and women. ROS can modulate cellular functions, and oxidative stress can disturb the intracellular milieu, resulting in diseased cells or endanger cell survival. Under normal conditions, antioxidants act to oppose ROS production, scavenging existing free radicals and promoting the repair of ROS-induced damage to cell structures. At controlled levels, oxidative stress facilitates some physiological reproductive functions but at higher levels it is implicated in pathological processes in the reproductive tract that contribute to infertility and poor pregnancy outcomes. As high levels of reactive oxygen species and low antioxidant status have been implicated in conditions contributing to infertility, treatment based on strategies to boost the exhausted antioxidant defense of the reproductive microenvironment is intuitive. Glutathione is a natural body antioxidant, which helps preserve all other antioxidants. It is present in both the male and female gametes and its level varies widely. This study reviews the role oxidative stress plays in both male and female infertility, and the antioxidant action of glutathione on infertility.