ArticleMolecular biology reports2026
Effects of tert-butylhydroquinone on cisplatin-induced neurotoxicity in rats.
Article in Molecular biology reports, 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
backgroundCisplatin (Cis) is a potent chemotherapy agent with limited clinical use due to serious side effects, including neurotoxicity. This study investigated the neuroprotective effects of tert-butylhydroquinone (TBHQ) against Cis-induced neurotoxicity. MATERIALS AND
methodsRats were randomly divided into five groups (n = 6 per group): Control, Cis, Vehicle, TBHQ, and Cis+TBHQ. Cognitive and behavioral changes were assessed using the Morris Water Maze (MWM) and the Open Field Test. Serum samples were analyzed for antioxidant/oxidant markers (SOD, CAT, GSH, and MDA), and hippocampal tissues were evaluated histopathologically and immunohistochemically (TNF-α, IL-6, and neurogranin).
resultsIn the MWM test, escape latency to the hidden platform on day 2 of training was significantly longer in the Cis group than in the control group (38.63 ± 15.77 s vs. 14.25 ± 5.82 s, p = 0.014). In contrast, TBHQ co-administration (Cis+TBHQ) alleviated these cognitive deficits, particularly during early learning, significantly reducing day 2 escape latency to 19.04 ± 7.77 s compared with the Cis group (38.63 ± 15.77 s, p = 0.044). Biochemically, Cis was associated with decreased serum SOD, CAT, and GSH and increased serum MDA (p < 0.05). Histopathologically, hemorrhagic foci were observed in the Cis group. Furthermore, immunohistochemical analysis revealed that Cis was associated with increased TNF-α and IL-6 immunoreactivity (p < 0.0001) and decreased neurogranin immunoreactivity (p < 0.0001).
conclusionCollectively, Cis administration causes potent neurotoxicity, severely impairs spatial learning, and alters plasticity-associated marker neurogranin and inflammatory markers. Specifically, TBHQ administration was associated with the attenuation of Cis-induced cognitive deficits and biochemical alterations. Given its defined profile, TBHQ may warrant further investigation for mitigating chemotherapy-induced neurotoxicity.
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