Ethanolic Citrus sinensis peel mitigates resorcinol bis(diphenyl phosphate)-induced testicular toxicity in Wistar rats through oxido-inflammatory pathways.

Salvia officinalis aqueous extract mitigates abamectin-induced testicular dysfunction in rats by targeting oxidative stress, mitochondrial fusion proteins, and key apoptotic regulators.

Abamectin (ABM) is a macrocyclic lactone insecticide that induces oxidative stress and testicular toxicity, but its specific effects on male reproductive function remain unclear. Here, we tested whether an aqueous extract of Salvia officinalis (S. officinalis) could mitigate ABM-induced testicular injury in adult male rats, focusing on mitochondrial fusion and apoptosis. Thirty-six rats were divided into six groups: control, S. officinalis extract (100mg/kg), low-dose ABM (0.5mg/kg), high-dose ABM (1mg/kg), S. officinalis + low-dose ABM, and S. officinalis + high-dose ABM, for 70 days. Our results showed that the extract was rich in total phenolics and flavonoids. The main phenolic compounds were ferulic acid, syringic acid, caffeic acid, p-coumaric acid, and α-tocopherol, while the main flavonoids were luteolin, 2'-hydroxyflavone, apigenin, and quercetin. Rats exposed to ABM had lower sperm concentration and motility, more abnormal sperm, and markedly lower serum levels of testosterone, luteinizing hormone, and follicle-stimulating hormone in a dose-dependent manner. Furthermore, testicular malondialdehyde and nitric oxide levels increased, whereas catalase activity, glutathione levels, and the activities of superoxide dismutase and glutathione S-transferase decreased. Gene expression analysis showed reduced mitofusin-1 and mitofusin-2 and increased p53 and caspase-9 expression. Notably, co-administration of S. officinalis with ABM improved sperm quality, hormone levels, antioxidant status, gene expression, and testicular tissue structure. Our findings highlight the protective mechanisms of S. officinalis, including enhancing antioxidant defenses, promoting mitochondrial fusion, and inhibiting the intrinsic apoptotic pathway. These results suggest that the S. officinalis extract could have therapeutic potential for ABM-induced male reproductive toxicity.

Black mulberry fruit extract attenuates valproic acid-induced toxicity by enhancing antioxidant defenses in FaO cells.

Findings indicate that black mulberry fruit extract partially mitigates VPA-induced hepatocellular injury, primarily by enhancing glutathione-dependent antioxidant defenses.

Protective effects of thymoquinone against hexavalent chromium-ınduced nephrotoxicity: a multiparametric evaluation of oxidative stress, ınflammation, ferroptosis- and apoptosis-related markers

Asiatic Acid Ameliorates Chlorpyrifos-Induced Toxicity in Rats: Biochemical and Histopathological Insights

ABSTRACT Introduction: Chlorpyrifos (CPF), one of the most widely used organophosphorus (OP) insecticides, exerts its toxic effects in part by inducing oxidative stress. Despite increasing recognition of natural antioxidants as potential countermeasures, the efficacy of asiatic acid (AA), a bioactive triterpenoid from Centella asiatica, against CPF-induced toxicity remains unexplored. This study aimed to investigate the protective effects of AA against CPF-incuded toxicity model in rats by analyzing biochemical and histological parameters in serum, liver, and brain tissues. Material and Methods: Adult male Sprague Dawley rats (n=30) were randomly divided into five groups: control, CPF (279 mg/kg, subcutaneously), and three AA-pretreated groups (35, 70, and 140 mg/kg, per os) for 14 days prior to CPF exposure. Oxidative stress markers [malondialdehyde (MDA), advanced oxidation protein products (AOPP)] and antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx)] were measured in serum, liver, and brain. Histopathological and immunohistochemical analyses assessed tissue injury and apoptotic responses. Results: AA administration significantly attenuated CPF-induced oxidative damage and restored antioxidant defenses in a dose-dependent manner. Histopathological analyses confirmed that AA mitigated hepatic and neuronal damage and preserved tissue architecture. Immunohistochemistry revealed that AA suppressed CPF-induced upregulation of the pro-apoptotic protein Bcl-2-associated X protein (Bax), indicating reduced apoptosis. Conclusion: This study provides the first demonstration that AA exerts robust systemic antioxidative, hepatoprotective, and neuroprotective effects against CPF-induced toxicity. These findings highlight AA’s therapeutic potential for mitigating organophosphate pesticide poisoning, warranting further translational research. Keywords: Asiatic acid, chlorpyrifos, hepatoprotection, neuroprotection, organophosphate toxicity, oxidative stress

Histo-protective efficacy of Withania somnifera (Ashwagandha) root extract against bisphenol A-induced testicular toxicity in rats

Background: Bisphenol A (BPA) is a high-volume synthetic endocrine disruptor widely used in polycarbonate plastics and epoxy resins. Its prevalence in food containers, water bottles, and can linings leads to continuous dietary exposure, raising significant public health concerns. This drives scientific interest in finding effective, natural protective agents. Withania somnifera (Ashwagandha), a prominent adaptogen in Ayurvedic medicine, is renowned for its cytoprotective, antioxidant, anti-inflammatory, and stress-alleviating properties, suggesting potential protective benefits against chemical toxicants. Aim: This study was designed to evaluate the histo-protective efficacy of a standardized Withania somnifera (Ashwagandha) root extract (WSRE) against BPA-induced testicular histopathological damage in rats. Methods: Forty adult male Wistar rats were divided into four groups (n=10): Group I (Control) received the vehicle only; Group II (BPA) received 200 mg/kg body weight/day of BPA orally; Group III (Ashwagandha) received 500 mg/kg body weight/day of Ashwagandha orally and Group IV (BPA plus Ashwagandha) received the same doses of both BPA and Ashwagandha at the aforementioned doses. The treatment continued for 60 consecutive days. Following sacrifice, the testes were immediately dissected out, fixed in Bouin\'s solution, and processed through dehydration and paraffin embedding. Five µm thick sections were obtained and stained with Hematoxylin and Eosin (H & E) to evaluate criteria such as germ cell degeneration, disorganization, vacuolization, and sloughing of spermatogenic cells. Results: Histopathological analysis of the BPA-only group revealed severe testicular injury, including marked distortion of tubule architecture, significant thinning and disorganization of the germinal epithelium, extensive vacuolization, and sloughing of spermatogenic cells into the lumen. Spermatogenesis was severely disrupted, with a notable absence of mature spermatozoa in many tubules. In contrast, the BPA plus Ashwagandha co-treatment group exhibited dramatic histoarchitectural preservation. Seminiferous tubules appeared near normal, with well-organized germinal epithelial layers containing all stages of spermatogenic cells. Degeneration, vacuolization, and cellular sloughing were minimal compared to the BPA-only group. Conclusion: Withania somnifera (Ashwagandha) root extract exhibits significant protective effects against the histopathological damage caused by BPA in rat testes. By maintaining the structural integrity of the germinal epithelium and ensuring the complete spermatogenic cycle, it validates its potential as a protective phytotherapeutic intervention for male reproductive toxicity.

Comparative Hepatoprotective Effects of Carica papaya, Azadirachta indica, and Allium sativum Extracts against Diethyl Nitrosamine-Induced Liver Injury in Wistar Rats

It is indicated that combining papaya, neem, and garlic extracts may provide greater hepatoprotection than administering the individual extracts against DEN-induced liver injury, and supports further mechanistic and preclinical evaluation of this polyherbal formulation before its potential therapeutic application in liver-disease management.