Mechanism associated with changes in male reproductive functions during ageing process.

Ageing is a natural process with physiological changes in different body parts and has been associated with decreased reproductive capacity. Factors such as imbalance in the antioxidant defence system, vascular diseases, diabetes mellitus, accessory reproductive glands infection, obesity as well as buildup of toxic substances play a role in age-related male reproductive malfunction. Age is inversely proportional to volume of semen, sperm count, sperm progressive motility, sperm viability, normal sperm morphology. The observed negative correlation between ageing and semen indices contributes to male infertility and reproductive decline. Normal levels of ROS, plays crucial role in facilitating sperm function, such as capacitation, hyper-activation, acrosome reaction as well as sperm-oocyte fusion; however, a substantial elevation in the endogenous level of ROS, especially in reproductive tissues, usually instigates destruction of sperm cells and heightened male infertility. Contrarily, antioxidants, such as vitamins C and E, beta-carotene, and micronutrients like zinc and folate, have been found by researchers to facilitate normal semen quality and male reproductive function. Furthermore, the role of hormonal imbalance as a result of the compromised hypothalamic-pituitary-gonadal axis, Sertoli and Leydig cells disorder, and nitric oxide-medicated erectile dysfunction during ageing cannot be undermined.

Dysthyroidism induces hepatorenal injury by modulating HSP70/HSP90 and VEGF signaling in male Wistar rats.

Thyroid hormones have been shown to promote the generation of reactive oxygen species (ROS), consumption of antioxidants, and induction of oxidative stress, which triggers the release of heat shock proteins (HSPs) and VEGF-dependent angiogenesis. The present study investigated the effect of altered thyroid states, hypothyroidism and hyperthyroidism on hepatic and renal functions, oxidative stress biomarkers, and hepatorenal expressions of HSP70, HSP90, and VEGF. Male Wistar rats were randomized into vehicle-treated control, carbimazole-induced hypothyroidism, or levothyroxine-induced hyperthyroidism. Altered thyroid states caused impaired hepatic and renal functions accompanied by elevated malondialdehyde and reduced glutathione content and superoxide dismutase and catalase activities in the hepatic and renal tissues. These derangements were associated with down-regulation of hepatic and renal HSP70 and HSP90 and upregulation of hepatic and renal VEGF expression. Findings of histopathological examinations of the hepatic and renal tissues align with the biochemical derangements observed.   This study reveals that dysthyroidism impairs hepatorenal function via induction of oxidative stress and modulation of HSP70/HSP90/VEGF signaling.