Promotion of oxidative stress: the disturbance of the pro-oxidant-antioxidant balance in favor of the former is defined as oxidative stress (Aly et al. 2010; Uchendu et al. 2012). The result of this multistep process is tissue damage that builds a pathway from the onset of tissue damage through disease to apoptosis (Agrawal and Sharma 2010). Oxidative stress-induced damage occurs through the production of reactive oxygen species (ROS) that include oxygen-derived free radicals such as superoxide anion, hydroxyl radical, and non-radical derivatives such as hydrogen peroxide ( Tebourbi et al. 2011; ROS induces alterations and damage to macromolecules such as lipids and proteins, the most common phenomenon being lipid peroxidation (Aly et al. 2010; Schneider and de Oliveira 2004). Oxidative destruction of lipids (lipid peroxidation) is a destructive and self-perpetuating chain reaction, releasing malonaldehyde as an end product (Vidyasagar et al. 2009). Pesticides are known to induce oxidative stress through the mechanisms shown in Fig.4. With the function of GABAergic inhibitory neurons impaired, hyperexcitation occurs (Coats 1990). Other mechanisms of action: Organophosphates inhibit the enzyme acetylcholinesterase in nerves, neuromuscular and glandular tissues where it plays an important role in cell-cell communication (Karalliedde et al. 2003). Organochlorines disrupt sodium-potassium flow across the axon membrane and induce a state of hyperexcitability in the central and peripheral nervous system leading to headache, dizziness, vomiting, and incoordination (Agrawal and Sharma 2010). They are presumed to involve binding to the picrotoxinin site in the γ-aminobutyric acid (GABA) chloride ionophore complex. This binding inhibits ClP f...... middle of paper ...... leads to a drop in the diffusing capacity of the lungs, and neonicotinoid insecticides have shown a relationship with lower lung volumes (total lung capacity, residual volume and functional residual capacity), indicative of restrictive lung disease (Hernandez et al. 2008). A progressive decline in CO2 diffusion capacity and arterial oxygen tension was also observed (Bismuth et al. 1982). Severe acute exposure to paraquat led to pulmonary edema and early lung damage within hours of ingestion (Nordquist et al. 1995; Honore et al. 1994). However, delayed toxic damage of pulmonary fibrosis, the usual cause of death, occurred most commonly 7-14 days after ingestion. The main 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).