Journal of Stress Physiology & Biochemistry, Vol. 21 No. 4 2025, pp. 32-44 ISSN 1997-0838
Original Text Copyright (cc) 2025  by  Karimov, Ryabova, Repina, Valova, Gizatullina, Yakupova, Smolyankin Khmel and Kurilov



ORIGINAL ARTICLE
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Chronic Stress Enhances Hepatotoxic Effects of Sorbic and Benzoic Acids in a Rat Model

D.O. Karimov1,2, Yu.V. Ryabova*1, E.F. Repina1, Ya.V. Valova1, A.A. Gizatullina1, T.G. Yakupova1, D. A. Smolyankin1, O.A. Khmel1, M.V. Kurilov1

1 Ufa research institute of occupational health and human ecology, Ufa, Russia
2 N.A. Semashko National Research Institute of Public Health, Moscow, Russia

*E-Mail:  ryabovaiuvl@gmail.com


Received May 30, 2025

Background: The individual effects of psychological stress and food preservatives on the liver—the body’s primary detoxification organ—are well-documented; however, little is known about their combined impact. The aim of this study was to evaluate the hepatic effects of sorbic and benzoic acid exposure in male rats subjected to chronic stress.

Results: Over a 28-day period, four groups of male rats were studied: Control, Chronic Stress, Preservatives (sorbic acid at 500 mg/kg and benzoic acid at 100 mg/kg), and a Combined Exposure group. Gene expression analysis revealed increased Sod1 expression under stress conditions, while Nqo1 and Hmox1 were significantly downregulated following preservative exposure and remained suppressed in the combined group. Biochemical analysis demonstrated reduced ALT, AST, and ALP activities across all experimental groups, with the most pronounced decreases observed under combined exposure. LDH activity was elevated under stress but declined when stress was coupled with preservative intake. Lipid metabolism was disrupted, as evidenced by decreased triglyceride levels and altered cholesterol concentrations. Total protein and albumin levels were significantly reduced only in the combined group. Despite preserved hepatic architecture, these molecular and biochemical changes suggest early signs of functional decompensation.

Conclusions: Co-exposure to chronic psychological stress and high doses of food preservatives resulted in a non-linear and potentially synergistic disruption of hepatic redox homeostasis, protein synthesis, and lipid metabolism. Further studies incorporating mitochondrial assessment, long-term exposure models, and quantitative interaction analysis are warranted to clarify the mechanisms underlying this toxicological synergy.

Key words:    chronic stress, food preservatives, liver, gene expression, Sod1, Hmox1, Nqo1, rats

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