title: Activation of inflammatory response and apoptosis of polymorphonuclear leukocytes in patients with argemone oil poisoning.
abstract: In the present study, the role of ROS and RNS in activation of inflammatory response and associated molecular events during apoptosis of polymorphonuclear leucocytes (PMNs) in patients from an outbreak of argemone oil (AO) poisoning leading to epidemic dropsy in Lucknow, India was undertaken. It was observed that generation of superoxide radical, nitrite formation and phagocytosis (103-429%) were significantly increased in PMNs of dropsy patients. Furthermore, activities of superoxide dismutase and glutathione peroxidase (GPx) (47-79%) were found to be increased while that of catalase and glutathione reductase (GR) (56-57%) were decreased. Lipid and protein oxidation, nitrotyrosine formation and 8-hydroxydeoxyguanosine (8-OHdG) excretion were significantly enhanced with concomitant depletion of GSH levels (67%) in dropsy patients. In addition, significant elevation of IL-6, IL-8 and TNF-alpha (68-406%) in plasma was observed. Apoptosis was enhanced (1.5 folds) with increased (2.0-3.6 folds) caspases 3, 8 and 9 activities along with DNA fragmentation (119%). The results suggest that generation of ROS and RNS along with enhancement of secretion of inflammatory mediators leading to DNA damage followed by apoptosis may have an effect on immune system, which in turn may be responsible for histopathological changes in target organs of dropsy patients.
authors.affiliation: Food Toxicology Division, Indian Institute of Toxicology Research (Formerly, Industrial Toxicology Research Centre), Post Box #80, Mahatma Gandhi Marg, Lucknow-226001, Uttar Pradesh, India.
authors.forename: Challagundla K
authors.initials: CK
authors.lastname: Babu
authors.forename: Kausar M
authors.initials: KM
authors.lastname: Ansari
authors.forename: Sanjay
authors.initials: S
authors.lastname: Mehrotra
authors.forename: Satyananda
authors.initials: S
authors.lastname: Patel
authors.forename: Madhu
authors.initials: M
authors.lastname: Dikshit
authors.forename: Mukul
authors.initials: M
authors.lastname: Das
mesh_terms: D017209:Apoptosis; D002374:Catalase / Q000378:metabolism; D004249:DNA Damage; D004487:Edema / Q000139:chemically induced / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D015227:Lipid Peroxidation; D009504:Neutrophils / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D010938:Plant Oils / Q000506:poisoning*; D050050:Protein Carbonylation; D026361:Reactive Nitrogen Species / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D010938:Plant Oils; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; C030610:argemone oil; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione