**6. Hormones involved in stress neurobiology and its mechanism of action**

Stress condition perturbs homeostasis of the human being gives large influences on human behavioural, endocrine system and cellular levels. Sympathetic (arousal) and parasympathetic (relaxation) nerve systems make up the autonomic nervous system. The automatic nervous system controls essential organs as well as visceral functions like respiration, digestion, circulation, and temperature regulation. In stress condition, the hypothalamus carries several distinct tasks which secretes arginine vasopressin, antidiuretic hormone, stimulates the hypothalamus gland. Scantamburlo et al. [41] claim that anterior pituitary gland results into production of ACTH in response to corticotropin releasing hormone (CRH) [40, 42]. Further, adrenal cortex (outer part) is stimulated by ACTH to release corticoids (glucocorticoids and mineralocorticoids). The main function of glucocorticoids is to release energy by conversion of glycogen into glucose and breakdown of fats into fatty acids and glycerol, which is needed to combat the negative consequences of a stressor [41, 43–45]. In addition, corticoids which inhibit the immune system, reduce hunger, aggravate gastrointestinal irritation, and associated feeling of depression and loss of control in stress conditions. On the other hand, aldosterone, a mineralocorticoid, encourages the retention of Na+ and the removal of K<sup>+</sup> . These reaction results into high blood pressure, heart rate, dilated pupils, constricted arteries to non-working muscles, and force to cardiac contraction. In addition, ADH known to maintain the blood pressure during stress when the body's equilibration is upset. Regulating fluid loss through the urinary system is the primary function of vasopressin (ADH), which is produced by the hypothalamus and released by the posterior pituitary. Further, the second significant alteration occurs during release of energy and distributions of energy to different organ system were needed. In addition, growth hormone (GH) and thyroid hormones played important role in stress condition. Due to stress condition, GH and thyroid hormones increased psychological stimuli in humans [46]. The thyroid gland secretes thyroxin and triiodothyronine which plays very important role

in the management of stress in the human body. Thyroid hormones' primary purpose is to boost basal metabolic rate, and raises heart rate and increase in the levels of catecholamines in stress situation. Despite, stress hormones, serotonin and melatonin are linked to mood. Depression is well connected with neurological problem and its reduction in stress in occupational setting is well reported [47–50].

Depression is well connected with neurological problem and its reduction in stress hormones in occupational setting are well reported [47–50].

### **7. Oxidative stress markers in mining workers**

The oxidants and antioxidants imbalance causes oxidative stress, which disrupts redox signalling and physiological function of the cell in humans. OS executed redox signalling-induced alterations, which might alter transcriptional activity, kinases networks, and apoptosis [51–55]. Studies reported that s-nitrosation, disulfide linkages, s-nitrosylation, S-glutathionylation, and sulfenylation proteins undergo discrete, reversible, and site specific alterations of cysteine residues to create redox signalling [56–58]. Exploring their potential clinical applications, nevertheless, continues to spark growing interest. Studies on oxidative stress markers in a variety of human diseases are being reported in published manuscripts. Thus, lot of focus on the analytical challenges needs to validate oxidative stress indicators in stressful condition [59, 60]. Although numerous indicators and techniques are employed but many of them lack strong correlations, fail to accurately reflect oxidative stress, and lack of specificity in occupational diseases in dust exposed workers. Recent studies reported that black lung in coal workers is caused due to bioavailable iron (BAI) present in the coal dust. The iron occurs in the coal dust reacts with the oxygen and oxygen peroxide and forms ROS. The ROS acts as a mediators which stimulate the activation of alveolar macrophage, immune cells and tend to release cytokines. The lung is a vulnerable organ to exogenous ROS because of its anatomy, function, and location where development of pulmonary diseases due to endogenous ROS. The lower respiratory tract becomes clogged with inflammatory mediators and activated phagocytotic cells, which produces ROS to protect respiratory system from environmental pollutant in the occupational settings. However, deposition of dust particle in alveolar macrophages activates the lung oxidative stress mechanism through the release of pro-inflammatory marker by ROS which damages DNA, protein, lipids etc. which causing lung disease in exposed workers. Studies confirmed that OS and the pro-inflammatory cytokines were involved in the progression of fibrotic lung disease in coal dust-induced pneumoconiosis, and progressive massive fibrosis (PMF) [61–64]. Recently, oxidative stress markers were reported in developed in-vitro model of alveolar epithelial (A549) and monocytic lung (U937) cell line for pneumoconiosis along with antioxidant enzymes. Oxidative stress parameter in the alveolar macrophage and lung epithelial cells exposed to coal dust results in the significant elevation in the oxidative stress markers NADPH, MPO, MDA and PC & reduction of antioxidant content (i.e. SOD, CAT and GSH). Results indicated that imbalance in the generation of ROS species and antioxidant enzyme could be one of the key payers to initiate the inflammation causing chronic tissue damage and fibrosis in the lung tissue. Coal exposure played a key role in the aetiology of asthma and chronic bronchitis (CB) [65–67]. By looking at oxidation target products, such as malonoaldehyde (end product of Lipid peroxidation), DNA damage, protein carbonyls, 8-isoprostane, DNA oxidation, and other oxidative stress markers generated by ROS can be evaluated either directly or indirectly. They can be used to evaluate

*Impact of Occupational Stress and Its Associated Factors on Cognitive, Hormonal and Stress… DOI: http://dx.doi.org/10.5772/intechopen.109587*

oxidative stress in humans since they are molecules whose structures have been altered by ROS. Antioxidant molecules including glutathione, protein thiols, and enzymatic antioxidant activity are further biomarkers of oxidative stress and key players in the body's antioxidant defence mechanism and a subject of extensive research [68, 69]. Finally, antioxidant enzymes, oxidants and proinflammatory cytokine markers may be used for OS in occupationally developed diseases in exposed workers.
