Please use this identifier to cite or link to this item: https://doi.org/10.1016/0041-0101(95)00128-X
Title: Pathological changes induced by an acidic phospholipase A2 from Ophiophagus hannah venom on heart and skeletal muscle of mice after systemic injection
Authors: Huang, M.-Z.
Gopalakrishnakone, P. 
Issue Date: 1996
Source: Huang, M.-Z.,Gopalakrishnakone, P. (1996). Pathological changes induced by an acidic phospholipase A2 from Ophiophagus hannah venom on heart and skeletal muscle of mice after systemic injection. Toxicon 34 (2) : 201-211. ScholarBank@NUS Repository. https://doi.org/10.1016/0041-0101(95)00128-X
Abstract: An acid phospholipase A2 (OHV A-PLA2) isolated from the venom of the king cobra (Ophiophagus hannah) was tested for its ability to cause pathological changes to myocardium, skeletal muscle and cardiac ganglia. White mice were injected intravenously with dose of 8 mg/kg or 4 mg/kg of OHV A-PLA2 and tissue samples were taken at 6 or 24 hr. Light microscopic examination failed to show significant changes in cardiac muscle and ganglia. Skeletal muscle showed myofibre degeneration and necrosis. Electron microscopic study revealed myodegeneration in cardiac and skeletal muscles, and reduction in synaptic vesicle population of preganglioinic nerve terminals in cardiac ganglia. Ultrastructural changes in tissues were dose related. The lower dose (4 mg/kg) of OHV A-PLA2 produced mild myocardial changes, the myofilaments were intact but contracted, and the A band and I band were skewed. OHV A-PLA2 caused myocardial degeneration at a higher dose of 8 mg/kg. The changes included dissolution of actin and myosin filaments, dilatation and disorganization of sarcoplasmic reticulum and degeneration of mitochondria. The skeletal muscle lesions were more severe than the myocardial changes. Some of the myofibrils were severely disorganized and lack typical striated appearance, sarcomeres disrupted, most of mitochondria were vesiculated and destroyed.
Source Title: Toxicon
URI: http://scholarbank.nus.edu.sg/handle/10635/33520
ISSN: 00410101
DOI: 10.1016/0041-0101(95)00128-X
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