Abstract

Stress can lead to various health problems. Exposure to stress is linked to several diseases including cancer, hypertension, diabetes, mental disorders, and heart attacks. Stress stimulates several pathways that produce free radicals, which increases oxidative stress. This results in functional and structural damage to organs, such as the brain, which is highly sensitive to oxidative stress Vitamin E is a naturally occurring potent antioxidant used for various purposes. The main purpose of the current study was to evaluate how vitamin E protects the brain and to what extent it affects antioxidant levels in rats subjected to two hours per day of immobilization stress, the form of stress with the strongest effect. The rats were immobilized by folding their limbs in and wrapping them in netting to prevent movement, while allowing their tails to be extended. The rats were then hung upside down. The effect of vitamin E was tested by intraperitoneally injecting rats with 40 mg/kg of vitamin E daily. Oxidative stress parameters were determined at the completion of the experiment. A dramatic decrease in malondialdehyde (MDA) levels and an increase in catalase (CAT), including glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), has been shown by vitamin E in the brain. The effects of vitamin E were significantly higher in the acute and chronic stress groups than in the control group. Vitamin E can decrease oxidative stress in stressed rats, indicating that it exerts therapeutic and protective effects owing to its antioxidant properties.

Introduction

Stress is a normal factor in everyday vernacular and a fundamental aspect of the human condition. Millions of missed working days are attributed to stress, which is acknowledged globally as the main contributor to chronic illnesses (e.g., Am. Psychol. Assoc. 2019, UK Health Saf. Executive 2019). It has been reported that stress affects every aspect of life. Furthermore, stress is known to have both direct and indirect negative effects on health via changes in neuroendocrine and autonomic functions (O’Connor et al., 2021).

Activation of the HPA axis, which causes an increase in corticosterone levels in the brain, is a key mechanism linked to stress-induced behavioral problems. Rapid depolarization caused by elevated corticosterone levels causes glutamate to be released into limbic and cortical areas. An increase in metabolic rate and mitochondrial dysfunction may result from glutamate overproduction. An increase in the metabolic rate results in a conflict between the generation of ROS and antioxidant system activity, which causes the generation of more free radicals. Nucleic acids, proteins, and lipids are just a few cellular components that oxidatively damage these free radical species oxidatively damage (Samarghandian et al., 2017).

Free radicals are associated with oxidative stress. Free radicals are highly reactive with unpaired electrons and atoms. An increase in the levels of antioxidants and free radicals can lead to oxidative stress.

Conclusion

Levels of the antioxidants GSH, SOD, and CAT in the brain were significantly higher in the vitamin E group than in the acute and chronic stress groups (controls). Vitamin E also significantly reduced MDA levels and oxidative stress in stressed rats. These findings suggest that vitamin E can prevent and relieve stress.