This study investigated the effects of Selenium (Se) on testis toxicity induced by Acrylamide (ACR) in rats. In our study, 50 male adult rats were used, and the rats were divided into five groups; control, ACR, Se0.5 + ACR, Se1 + ACR, and Se1. Se and ACR treatments were applied for 10 days. On the 11th day of the experimental study, intracardiac blood samples from the rats were taken under anesthesia and euthanized. Sperm motility and morphology were evaluated. Dihydrotestosterone, FSH, and LH levels in sera were analyzed with commercial ELISA kits. MDA, GSH, TNF‐α, IL‐6, and IL‐1β levels and SOD, GPx, and CAT, activities were measured to detect the level of oxidative stress and inflammation in rat testis tissues. Expression analysis of HSD17B1, StAR, CYP17A1, MAPk14, and P‐53 as target mRNA levels were performed with Real Time‐PCR System technology for each cDNA sample synthesized from rat testis RNA. Testicular tissues were evaluated by histopathological, immunohistochemical, and immunofluorescent examinations. Serum dihydrotestosterone and FSH levels decreased significantly in the ACR group compared to the control group, while LH levels increased and a high dose of Se prevented these changes caused by ACR. A high dose of Se prevented these changes caused by ACR. ACR‐induced testicular oxidative stress, inflammation, apoptosis, changes in the expression of reproductive enzymes, some changes in sperm motility and morphology, DNA, and tissue damage, and Se administration prevented these pathologies caused by ACR. As a result of this study, it was determined that Se prevents oxidative stress, inflammation, apoptosis, autophagy, and DNA damage in testicular toxicity induced by ACR in rats.

Bisphenol A (BPA), commonly found in plastic containers and epoxy resins used for food products, presents substantial health risks, particularly in relation to hepatic toxicity. This study investigates BPA-induced liver damage and explores the mechanistic dose-dependent protective effects of P-coumaric acid (PCA). 50 male rats were divided into control, BPA-treated, BPA + PCA50, BPA + PCA100, and PCA100 groups. BPA exposure for 14 days induced oxidative stress, evidenced by elevated malondialdehyde levels and decreased activities of antioxidant enzymes (superoxide dismutase, glutathione peroxidase, and catalase). Higher doses of PCA effectively mitigated these effects by restoring redox balance and enhancing antioxidant enzyme activities. Additionally, BPA disrupted inflammation and apoptosis pathways, inhibiting anti-inflammatory markers and interfering with the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) pathway. PCA exhibited dose-dependent protection against these disruptions. Computational analyses revealed that BPA inhibits cyclooxygenase-1 through stable hydrogen bonding with threonine at position 322. PCA’s dual protective effect was confirmed by attenuating inflammatory pathways, including TNF-α inhibition and suppression of the Kelch-like ECH-associated protein 1 (KEAP1) and Nrf2 signaling pathway. Histopathological assessments confirmed that PCA alleviated significant hepatic damage induced by BPA. Immunohistochemical and immunofluorescence analyses further supported PCA’s protective role against BPA-induced apoptosis and cellular hepatotoxicity. These findings underscore PCA’s protective potential against BPA-induced hepatotoxicity and highlight novel mechanistic interactions that warrant further investigation in applied nutritional biochemistry.

This study investigates the molecular effects of Acrylamide (ACR)-induced kidney damage and the potential protective role of Gallic acid (GA). Forty male rats were divided into five groups: Control, ACR, ACR+GA50, ACR+GA100, and GA100. The ACR groups received a daily oral dose of 50 mg/kg, while GA groups received 50 or 100 mg/kg oral doses for 14 consecutive days. On the 15th day, the animals were euthanized, and kidney samples were collected. The MDA, GSH, SOD, GPx, and CAT oxidative stress parameters were measured. The renal inflammatory response was evaluated by measuring the level of TNF-α, IL-1β, IL-6, NF-κB, COX-2, and IL-10. The downstream pro-apoptotic signaling pathway was resolved by measuring the levels of p38 MAPK and p53. The ACR induced renal oxidative stress with aggravated lipid peroxidation as revealed by the reduction in the levels GSH, SOD, GPx, and CAT of antioxidants while over-increase in the level of MDA, respectively. The levels of IL-1β, IL-6, NF-kB, COX-2 pro-inflammatory mediators as well as the p38 MAPK and p53 pro-apoptotic intermediates were further elevated. This increase in inflammatory response was met with marked decrease in anti-inflammatory IL-10 level. However, GA treatments- in dose dependent manner- had been demonstrated to effectively mitigate oxidative stress and reduce inflammatory responses, while also enhancing the cellular anti-inflammatory defense mechanisms. The GA can be considered as a novel protective antioxidant, anti-apoptotic drug against ACR-induced nephrotoxic insult. Further study should be performed to estimate the exact effective dose.