| Literature DB >> 3190455 |
N Hieda1, S Sugiyama, Y Ogawa, T Ito, T Satake, T Ozawa.
Abstract
This study was designed to clarify the role of phospholipase in the mechanism of plasmocid-induced mitochondrial dysfunction in the rat heart. Rats were divided into two groups: the control group, untreated; and the plasmocid group, in which plasmocid (30 mg/kg) was injected subcutaneously. In each group, the level of lipid peroxides and the phospholipase activity in heart homogenate were measured, and mitochondrial function (respiratory control index and the rate of oxygen consumption in State III) was determined polarographically. The activity of lysosomal enzymes (N-acetyl-beta-glucosaminidase and beta-glucuronidase) were also measured. The plasmocid group showed significant increases in lipid peroxide levels and phospholipase activity. Administration of plasmocid also caused mitochondrial dysfunction, while no significant changes were observed in the lysosomal enzyme activity of either group. These results suggested that plasmocid-induced mitochondrial dysfunction is based on the degrading of phospholipids by membrane bound phospholipase, and that lysosomal enzymes are unlikely to be involved in plasmocid-induced mitochondrial dysfunction.Entities:
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Year: 1988 PMID: 3190455 DOI: 10.1007/bf00316256
Source DB: PubMed Journal: Arch Toxicol ISSN: 0340-5761 Impact factor: 5.153