The functions of mammalian testis are temperature-sensitive. There are various testicular factors, which express in response to heat as a mechanism of defence. PGC-1α and HSP70 have poetical role in the protection from oxidative stress in various tissues, including testis. The expression of PGC-1α and HSP70 has been shown in the testis, and it has also been documented that heat modulates the expression of PGC-1α and HSP70. However, heat-dependent changes in the localisation and expression of PGC-1α have not been investigated so far. Thus, we studied the expression and localisation pattern of PGC-1α in the testis of heat-treated mice along with marker of proliferation (PCNA, GCNA), serum testosterone levels, MDA levels and HSP70. The results showed a significant increase in PGC-1α and HSP70 and MDA levels in the testis of heat-treated mice along with a decrease in PCNA, GCNA and serum testosterone levels. The immunolocalisation study showed intense immunostaining of PGC-1α in the Leydig cell and germ cells of the heat-treated testis, with pronounced damaged in the histoarchitecture. The results showed that increase expression of PGC-1α in germ cells and Leydig cells of testis could be a counter mechanism to cope up with oxidative stress in coordination with HSP70.

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Cadmium (Cd) is one of the heavy metal pollutants present in the environment due to human intervention. It is well known that Cd causes toxicological effects on various organs, including the testes. Morin hydrate is a plant‐derived bioflavonoid with antioxidant, anti‐inflammatory, and anti‐stress properties. Thus, the question can be raised as to whether Morin has an effect on Cd‐intoxication‐induced testicular impairment. Therefore, the aim of this study was to investigate the role of Morin on Cd‐mediated disruption of testicular activity. Mice were divided into three groups: group 1 served as the control group, group 2 was given Cd (10 mg/kg) orally for 35 days, and group 3 was given Cd and Morin hydrate (100 mg/kg) for 35 days. To validate the in vivo findings, an in vitro study on testicular explants was also performed. The results of the in vivo study showed that Cd‐intoxicated mice had testicular disorganization, reduced circulating testosterone levels, decreased sperm density, and elevated oxidative stress and sperm abnormality. The expression of the germ cell proliferation marker, germ cell nuclear acidic protein (GCNA), and adipocytokine visfatin were also downregulated. It was observed that Morin hydrate upregulated testicular visfatin and GCNA expression in Cd‐intoxicated mice, along with improvement in circulating testosterone, testicular histology, and sperm parameters. Furthermore, the in vitro study showed that Cd‐mediated downregulation of testicular visfatin and GCNA expression, along with the suppressed secretion of testosterone from testicular explants, was normalized by Morin treatment, whereas visfatin expression was not. Overall, these data indicate that environmental cadmium exposure impairs testicular activity through downregulation of visfatin and GCNA expression, and Morin might play a protective role against Cd‐induced testicular toxicity.

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The seed of Cycas pectinata is widely used in traditional practices in the Northeastern region of India for diverse purposes along with improving testicular functions. Thus, it may be hypothesized that the phytochemicals of C. pectinata seed could modulate testicular steroidogenesis. Therefore, we have investigated the effects of C. Pectinata seed extract (CPE) on testicular steroidogenesis by using in vivo and in vitro approaches. We have also performed the molecular docking of phytochemicals with some steroidogenic markers based on the identified phytochemicals from our previous study. The in vivo treatment of CPE increased the circulating estrogen and decreased circulating testosterone. The in vitro treatment of CPE also showed increased secretion of estrogen which can be suggested due to an increase in the aromatase (CYP19A1) activity. Our results also showed that the expression and localization of CYP19A1 were elevated by the CPE. The treatment of CPE also showed an accumulation of cholesterol in the testis, which could enhance testicular steroidogenesis. The other steroidogenic markers like 3βHSD, StAR, and LHR were upregulated by the CPE. Twelve compounds exhibited binding energy in the range of -10.0 to -8.0 kcal/mol with CYP19A1. Our data from in vitro, in vivo, and docking studies, showed that phytochemicals of CPE could modulate testicular steroidogenesis.