Aug 2026· Ankara Üniversitesi Veteriner Fakültesi Dergisi· 0 citations· 41 references
TL;DR
It is indicated that chlorogenic acid influences testicular oxidative status and ferroptosis-related gene responses under acrylamide exposure, supporting its potential relevance as a dietary component for acrylamide-associated reproductive oxidative stress.
Abstract
Acrylamide is a processing contaminant formed during high-temperature cooking of carbohydrate-rich foods and has been associated with impaired male reproductive function. This study aimed to determine the effects of chlorogenic acid on testicular lipid peroxidation and ferroptosis-related gene expression (GPX4, SLC7A11, and TFRC) in rats with acrylamide-induced testicular toxicity. Thirty-two male Wistar albino rats were randomized into four groups (n=8 per group): control, acrylamide-treated (ACR), chlorogenic acid–treated (CGA), and acrylamide + chlorogenic acid (ACR+CGA). Treatments were administered once daily by oral gavage for 28 days. At the end of the experimental period, testicular tissues were analyzed for malondialdehyde as an index of lipid peroxidation and for RT-qPCR assessment of GPX4, SLC7A11, and TFRC. Acrylamide exposure significantly increased malondialdehyde levels compared with controls, indicating enhanced lipid peroxidation. Conversely, chlorogenic acid co-treatment partially attenuated this increase, restoring malondialdehyde levels to near-control values. Gene expression analysis revealed that GPX4 was significantly upregulated 2.17-fold in the CGA group, while TFRC was significantly upregulated in both the CGA (2.66-fold) and ACR+CGA (2.34-fold) groups relative to the control, suggesting a potential adaptive response within the ferroptosis regulatory network. In silico protein-protein interaction network and functional enrichment analyses suggested that the GPX4 and TFRC interaction network is enriched for pathways related to selenoprotein metabolism and cellular iron handling. These findings indicate that chlorogenic acid influences testicular oxidative status and ferroptosis-related gene responses under acrylamide exposure, supporting its potential relevance as a dietary component for acrylamide-associated reproductive oxidative stress.
Acrylamide (Acr) is a widely encountered environmental and dietary toxicant known to induce oxidative stress and disrupt male reproductive function. Leydig cells, due to their high metabolic activity and mitochondrial dependence, are particularly vulnerable to redox imbalance. N-acetylcysteine (Nac), a thiol-containing antioxidant and glutathione precursor, has been extensively studied for its cytoprotective properties. However, its modulatory effects on Acr-induced toxicity in Leydig cells and its pharmacodynamic interaction profile remain incompletely characterized. In this study, TM3 Leydig cells were exposed to Acr in the presence or absence of Nac. Cell viability was assessed by MTT assay, and chemical interaction profiles were evaluated using ZIP, Bliss, and Chou-Talalay combination index analyses. Oxidative stress parameters, including intracellular reactive oxygen species (ROS), lipid peroxidation, antioxidant enzyme activities (SOD, CAT, GPx), and glutathione levels, were measured. Apoptotic responses were analyzed through double fluorescence staining, RT-qPCR of apoptosis-related genes (Bax, Bcl2, Casp3, Trp53), and Western blot analysis of CASP3 protein expression. Acr exposure significantly reduced cell viability, increased ROS and lipid peroxidation levels, suppressed antioxidant defenses, and activated the mitochondrial apoptotic pathway. Nac treatment markedly improved cell viability, restored antioxidant capacity, reduced oxidative stress markers, and suppressed p53/Bax/Casp3-mediated apoptotic signaling. Combination analyses revealed an antagonistic interaction profile, indicating that Nac biologically limits Acr-induced cytotoxicity. Collectively, these findings demonstrate that Nac exerts protective effects in Leydig cells by modulating redox homeostasis and mitochondrial apoptosis, suggesting its potential as a protective regulator against Acr-induced reproductive toxicity.
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Pentadecafluorooctanoic acid (PFOA), a persistent environmental pollutant, has been implicated in hepatotoxicity through mechanisms involving oxidative stress, inflammation, and metabolic dysfunction. This study investigated the hepatoprotective effects of chrysin against PFOA-induced liver injury in male Wistar rats. Twenty-five male Wistar rats were randomly divided into five groups (n = 5): control (20% dimethyl sulfoxide), PFOA (5 mg/kg), PFOA + chrysin (25 mg/kg), PFOA + chrysin (50 mg/kg), and chrysin only (50 mg/kg). Treatments were orally administered for 14 days. Serum and hepatic biomarkers of liver function, oxidative stress, inflammation, membrane integrity, and energy metabolism were evaluated using standard biochemical assays and enzyme-linked immunosorbent assay methods. PFOA exposure significantly (p < 0.05) increased serum liver enzymes (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase), lipid peroxidation marker (malondialdehyde), and pro-inflammatory cytokines (interleukin 1 beta and interferon gamma), while significantly reducing antioxidant parameters (glutathione, catalase, superoxide dismutase, glutathione peroxidase, and glutathione-S-transferase, nitric oxide (NO), and membrane-bound enzyme activities, including adenosine triphosphatase (ATPase), Ca2+/Mg2+ ATPase, and 5’-nucleotidase. Chrysin treatment at both 25 and 50 mg/kg significantly (p < 0.05) ameliorated these alterations in a dose-dependent manner, with the 50 mg/kg dose showing greater protective efficacy. The findings indicate that PFOA-induced hepatotoxicity is associated with oxidative stress, inflammation, and metabolic dysfunction, whereas chrysin pre-treatment restores antioxidant defenses, attenuates inflammatory responses, and normalizes membrane-associated enzyme activities. Overall, chrysin demonstrates potent protective potential against PFOA-induced liver injury and may serve as a promising therapeutic candidate for environmental toxin-associated hepatotoxicity.
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