ORIGINAL
ARTICLE |
Data source : Google Scholar QueryDate : 2016-12-24 Cites : 0 |
Vinay Kumar Singhǂ1,3, Saurabha Srivastavaǂ2, Kaleshwar Prasad Singh1*
1Dept.
of Microbiology, CSMMU (KGMU), Lucknow, U.P. India
2Dept.
of Biochemistry, Faculty of Science, BHU, Varanasi, U.P. India
3Department
of Medical Biochemistry, Facility of Medicine, NIMS University,
Rajasthan, Jaipur, India
ǂ
authors are equally contributed.
*E-Mail: malaria.microbiology@gmail.com
Received July 1, 2011
Free radicals are often formed as necessary intermediates in a variety of biochemical reactions but when generated in excess or not appropriately controlled, they can wreak havoc on a wide range of macromolecules. Of the several free radicals generated in the biological system, the reactive oxygen species such as .OH are highly toxic and injurious agents causing irreparable tissue damage. At a point of time in the intraerythrocytic stage of P. yoelii infection, digestion of hemoglobin releases free heme, which in the presence of transition metal ion (Fe+3 / Fe+2) generates .OH and notably H2O2, a potent reactive oxygen intermediate (ROI) that causes lipid-peroxidation. Owing to its lipophilic nature, free heme intercalates in the lipid bilayer, disrupts the integrity of the membrane and hence destabilizes the cytoskeleton. Following lipid peroxidation of the food vacuolar membrane, in the course of malarial infection, free heme comes out from food vacuole. The current paper deals with a study on the effect of free heme on the various membranes viz. RBC membrane, food vacuole membrane and parasite membrane particularly during the intraerythrocytic stage of malarial infection.
Key words: Plasmodium yoelii, Lipid-peroxidation, Reactive Oxygen Intermediate (ROI), Heme toxicity