Stress And Oxidative Stress

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Oxidative stress promotion: Disturbance of the prooxidant-antioxidant balance in favour of the former is termed as oxidative stress (Aly et al. 2010; Uchendu et al. 2012). The outcome of this multistep process is tissue damage which builds a path from the onset of tissue damage through diseases to finally apoptosis (Agrawal and Sharma 2010). Damage induced by oxidative stress occurs through the production of reactive oxygen species (ROS) which includes oxygen derived free radicals such as superoxide anion, hydroxyl radical and non radical derivatives as hydrogen peroxide (Tebourbi et al. 2011; Verma et al. 2007). ROS induces alterations and damage to macromolecules like lipids and proteins, most common phenomena being lipid peroxidation (Aly et al. 2010; Schneider and de Oliveira 2004). The oxidative destruction of lipids (lipid peroxidation) is a destructive, self-perpetuating chain reaction, releasing malonaldehyde as the end-product (Vidyasagar et al. 2009). Pesticides are known to induce oxidative stress by mechanisms shown in Fig.4. With the function of the GABA-ergic inhibitory neurons impaired, hyperexcitation results (Coats 1990).
Other mechanisms of action: Organophosphates inhibit enzyme acetylcholinesterase in nerves, neuromuscular and glandular tissues where is plays important role in cell to cell communication (Karalliedde et al. 2003).
Organochlorines disrupt the sodium- potassium flow across the axon membrane and induce hyperexcitable state in central and peripheral nervous system leading to headache, dizziness, vomiting and incoordination (Agrawal and Sharma 2010). They are purported to involve binding at the picrotoxinin site in the y-aminobutyric acid (GABA) chloride ionophore complex. This binding inhibits ClP f...

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... lead to a fall in the diffusing capacity of the lungs and neonicotinoid insecticides showed a relationship with lower pulmonary volumes (total lung capacity, residual volume, and functional residual capacity), suggestive of restrictive lung disease (Hernandez et al. 2008). A progressive decline in CO2 diffusion capacity and arterial oxygen tension has also been observed (Bismuth et al. 1982).
Severe acute exposure to paraquat led to pulmonary edema and early lung damage within few hours of ingestion (Nordquist et al. 1995; Honore et al. 1994). However, delayed toxic damage of pulmonary fibrosis, the usual cause of death, most commonly occurred 7-14 days after the ingestion. The primary mechanism of action of paraquat poisoning on the respiratory system is through the generation of free radicals with oxidative damage to lung tissue (Giulivi et al. 1995; Pond 1990).

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