Investigating the Protective Effect of Regular Aerobic Exercise and Benfotiamine on Improving Oxidative Brain Damage Caused by Occupational Noise in Male Mice

Abstract

Background and purpose: Exposure to noise leads to the production of reactive oxygen species (ROS) or free radicals in the brain. Even a slight increase in free radical levels in brain cells can disturb the central nervous system's structure and contribute to related diseases, including Alzheimer's disease. Therefore, this study aimed to investigate the protective effects of four weeks of regular aerobic training and benfotiamine supplementation on noise-induced oxidative stress in the brains of mice. Materials and methods: Forty male mice were randomly divided into five groups: a control group, a noise-exposed group subjected to occupational noise (100 dB, 4 hours per day), a noise+exercise group, a noise+benfotiamine group, and a noise+exercise+benfotiamine group. All animals, except those in the control group, were exposed to daily occupational noise emitted from a loudspeaker. After noise exposure, benfotiamine (200 mg/kg) was administered via gavage to two groups of mice. The training groups then performed aerobic exercise on a treadmill (5 days per week, 30 minutes per day at 12 m/min) according to protocol. All interventions were performed for four consecutive weeks. Seventy-two hours after the last exercise session, the animals were anesthetized, and brain tissues were immediately collected and homogenized for further evaluation. Brain tissue levels of ROS, malondialdehyde, protein carbonyl, reduced glutathione, and total antioxidant capacity—markers of oxidative stress—were measured using biochemical methods. One-way analysis of variance and Tukey's post hoc tests were used to analyze the data. Results: The results showed that, compared to the control group, daily exposure to occupational noise for four hours significantly increased levels of ROS, malondialdehyde, and protein carbonyl (P0.05). Daily administration of benfotiamine supplements led to reductions in ROS and malondialdehyde levels and an increase in reduced glutathione in brain tissues of noise-exposed mice compared to the noise group (P0.05). Compared to the noise group, combining aerobic exercise with benfotiamine consumption significantly reduced ROS and protein carbonyl levels and increased glutathione in the brain tissue of noise-exposed animals (P0.05). Conclusion: The results of this study indicate that benfotiamine, as an effective antioxidant, may have a protective and preventive role in reducing oxidative stress in brain tissue caused by occupational noise in mice. Daily benfotiamine supplementation combined with aerobic exercise may be an effective strategy for preventing oxidative disorders related to occupational noise exposure by inhibiting ROS production and improving certain oxidative stress markers. Further studies are needed to clarify the mechanisms underlying the combined effects of benfotiamine and aerobic exercise in reducing noise-induced oxidative stress.

Keywords

• noise
• exercise training
• antioxidant
• benfotiamine
• neurotoxicity