Cortisol, β-endorphin and oxidative stress markers in healthy medical students in response to examination stress. Kyaimon Myint 1* , R Jayakumar 2 , See-Ziau Hoe 1 , MS Kanthimathi 2,3 , Sau-Kuen Lam 1 1 Department of Physiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia 2 Department of Molecular Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia 3 University of Malaya Centre for Proteomics Research (UMCPR), University of Malaya, 50603 Kuala Lumpur, Malaysia Abstract The psychosomatic connection pertaining to the relationship between perceived stress and the milieu intérieur that must be evident during a naturalistic stressor event is not well explored. Objective: This study therefore examines the interrelationship between perceived stress scores, endocrine levels and oxidant-antioxidant activities under the duress of examination stress, an appropriate example of a naturalistic stressor. Materials and methods: Apparently healthy year one medical students participated. Results: Examination stress induced significant increases in perceived stress scores (p<0.001), serum cortisol (p<0.05) and plasma β-endorphin (p<0.05) levels, and erythrocyte lipid peroxidation (p<0.001), but a significant (p<0.001) decrease in the antioxidant superoxide dismutase activity. In addition, during the examination, the perceived stress scores were found to be correlated positively with lipid peroxidation (r 2 =0.23; p<0.01) but negatively with β-endorphin (r 2 =0.14; p<0.05). After the examination, the perceived stress scores correlated positively only with cortisol (r 2 =0.09; p<0.05). Conclusion: Sitting for an examination increases cortisol secretion, as well as, β-endorphin levels and induces oxidative stress. The high levels of β- endorphin appear to have an ameliorating effect on cortisol and the perception of stress. This finding awaits further investigation. Keywords: Examination stress, Perceived stress scores, Cortisol, β endorphin, Oxidative stress markers. Accepted on February 07, 2017 Introduction In daily life, all organisms are faced with various types of day- to-day stresses. Some organisms can cope well with the stress stimuli while in others repeated daily stress could lead to derangement of the neuroendocrine coping mechanism and balance between pro- and anti-oxidants, producing a wide range of detrimental effects on the physiological and psychological homeostasis. It is well-known that the hypothalamo-pituitary-adrenal (HPA) axis is highly sensitive to and easily activated by various stressors. The axis responds by releasing corticotrophin- releasing hormone (CRH) from the hypothalamus and the consequent adrenocorticotrophic hormone (ACTH) from the anterior pituitary gland. The circulating ACTH then acts on the adrenal cortex causing the release of glucocorticoids (mainly cortisol), the hormonal end-products of the HPAaxis [1], and it is intricately involved in the adaptation to stress. In the 1970s, beta-endorphin (β-endorphin), a cleavage product of a precursor hormone for ACTH, was discovered by Li and Chung [2]. This compound is an endogenous opiate and is believed to modulate pain, boost the immune system, promote the feeling of wellbeing, and increase relaxation. However, little is known about the role of β-endorphin in acute naturalistic stress [3-6]. Thus, more studies are called for to determine whether endorphins might be released during times of stress that could have significant roles in preventing wear and tear of the body. Since the pioneering work of Gerschman in the 1950s on oxygen poisoning [7], the role of free radical reactions in humans has been critically reappraised. In the human body, high levels of constantly formed free radicals and other reactive oxygen species (ROS) such as superoxide anion (O 2 ˙ −), hydrogen peroxide (H 2 O 2 ) and hydroxyl radicals ( ˙ OH) are involved in the generation of cascade reactions that attack cell membrane phospholipids and induce membrane lipid peroxidation. In particular, the well-characterised product of lipid peroxidation, malondialdehyde (MDA), can cause damage to proteins and DNA resulting in cellular apoptosis [8]. Hence, protection against and prevention of the consequences ISSN 0970-938X www.biomedres.info Biomed Res- India 2017 Volume 28 Issue 8 3774 Biomedical Research 2017; 28 (8): 3774-3779