BLD 204 Lecture Notes - Lecture 5: Phospholipase A2, Lipid Bilayer, Sphingomyelin

• School: MSU
• Department: Biomedical Laboratory Diagnostics
• Course: BLD 204
• Professor: R.Morris

Document Summary

Mechanisms of cell injury: increase intracellular ca2: excess calcium causes activation of enzymes:phospholipases: degrade phospholipids --> membrane damage ("m"). Proteases: digest proteins (within membranes, within the cell, etc. ) Changes permeability within mitochondrial membrane--> inability to produce atp. Sources of excess calcium: malfunction of sodium/calcium pump on membrane surface, endoplasmic reticulum, mitochondria. Most things that can cause cell injury will cause injury to mitochondria. Breakdown of phospholipids: phospholipase a2 and sphingomyelin pathways may break down lipids. These lipid breakdown products, free fatty acids and ceramide, may also damage mitochondria. What happens when there is a decrease in oxygen supply? (notepool: oxidative phosphorylation pathway needs oxygen, when there is not enough oxygen --> mitochondrial damage and dysfunction --> Atp generation impaired -->production of ros --> leak out of cell --> cause damage to cellular components --> necrosis. Depletion of atp and lack of atp synthesis are frequently caused by chemical injury as well as hypoxia.