ArticlePurinergic signalling2026
Modulation of P2X7-driven purinergic signaling and NLRP3 inflammasome activation underlies the hepatoprotective effects of coenzyme Q10 against glyphosate-based herbicide exposure.
Article in Purinergic signalling, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The widespread use of glyphosate-based herbicides (GBHs), including formulations such as Roundup, has raised toxicological concern due to their capacity to induce oxidative stress, inflammatory signaling, and mitochondrial dysfunction leading to hepatocellular injury. The present study investigated whether coenzyme Q10 (CoQ10) confers hepatoprotection against GBH exposure through modulation of oxidative stress-driven P2X7/NLRP3 inflammasome signaling and downstream inflammatory and apoptotic pathways. Fifty male ICR mice were randomly assigned to five groups (control, sham, CoQ10, GBH, and GBH + CoQ10) and treated by oral gavage for 49 days with Roundup (500 mg/kg/day), CoQ10 (200 mg/kg/day), or their combination. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) levels were assessed along with hepatic oxidative stress markers malondialdehyde (MDA), glutathione (GSH), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI). Liver injury was evaluated histologically, while proliferative and inflammatory responses were analyzed by immunohistochemistry. Hepatic expression of inflammasome- and apoptosis-related genes (P2X7, NLRP3, caspase-1, IL-1β, NF-κB, TNF-α, caspase-3, and Bcl-2) was quantified by RT-qPCR. GBH exposure markedly increased serum liver enzymes, disrupted oxidative balance, and induced necroinflammatory liver injury with Kupffer cell activation and hepatocellular nuclear alterations. These changes were associated with increased PCNA and COX-2 immunoreactivity, activation of the P2X7-NLRP3 inflammasome axis, and a proapoptotic transcriptional profile. CoQ10 coadministration attenuated biochemical, histopathological, inflammatory, and apoptotic alterations, although several parameters remained incompletely normalized. In conclusion, CoQ10 provides partial but meaningful hepatoprotection against GBH-induced liver injury, highlighting P2X7-NLRP3-linked oxidative inflammation as a key mechanism in GBH hepatotoxicity.
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