Palladium chloride-induced testicular damage in rats: Histopathology, oxidative stress, ER stress, and Nrf2/HO-1 signaling and the protective role of quercetin.
TL;DR
Overall, the findings indicate that Que mitigates PdCl₂-induced testicular injury, and that this protection may be associated with antioxidant, anti-inflammatory, anti-apoptotic, ER stress-related, and Nrf2/HO-1-associated responses rather than direct proof of pathway activation.
Abstract
The present study aimed to evaluate the protective potential of quercetin (Que), a flavonoid recognized for its antioxidant and anti-inflammatory activities, against palladium chloride (PdCl₂)-induced testicular toxicity. Twenty-four male Wistar rats were assigned to Control, Que (30 mg/kg), PdCl2 (8 mg/kg), and Que + PdCl2 groups for 28 days. PdCl₂ exposure was associated with reduced serum testosterone, LH, and FSH levels, impaired sperm quality, histopathological injury, increased oxidative stress and oxidative DNA damage, and diminished antioxidant capacity. These changes were accompanied by reduced Nrf2 and HO-1 levels, increased IL-6 and IL-1β concentrations, enhanced TNF-α immunoreactivity, and increased immunoreactivity of apoptosis and ER stress-related markers. Que co-treatment partly counteracted these alterations, improving redox balance, hormone levels, sperm parameters, and tissue morphology. Overall, the findings indicate that Que mitigates PdCl₂-induced testicular injury, and that this protection may be associated with antioxidant, anti-inflammatory, anti-apoptotic, ER stress-related, and Nrf2/HO-1-associated responses rather than direct proof of pathway activation.