Once initiated, how does toxic tissue injury expand?

Trends in Pharmacological Sciences

Volumn 33, Issue 4, 2012, Pages 200-206

  Mehendale, Harihara M ^a  

^a UNIVERSITY OF LOUISIANA AT MONROE   (United States)

Author keywords

acetaminophen; calpain; carbon tetrachloride; death proteins; secretory phospholipase A 2; thioacetamide

Indexed keywords

ACID PHOSPHATASE; ALANINE AMINOTRANSFERASE; CALPAIN; CARBON TETRACHLORIDE; CATHEPSIN D; CYCLOOXYGENASE 1; CYCLOOXYGENASE 2; CYTOCHROME P450 2E1; DAXX PROTEIN; DEOXYRIBONUCLEASE I; INTERLEUKIN 1; INTERLEUKIN 8; PARACETAMOL; PHOSPHOLIPASE A2; PROSTAGLANDIN E2; SECRETORY PHOSPHOLIPASE A2; THIOACETAMIDE; TUMOR NECROSIS FACTOR ALPHA;

ALANINE AMINOTRANSFERASE BLOOD LEVEL; CATALYSIS; CELL DEATH; CYTOKINE PRODUCTION; CYTOLYSIS; DISEASE COURSE; DOSE RESPONSE; DRUG HALF LIFE; DRUG TRANSFORMATION; ENZYME ACTIVITY; EXTRACELLULAR MATRIX; INFLAMMATION; LETHAL DOSE; LIPID PEROXIDATION; LIVER NECROSIS; LIVER TOXICITY; NONHUMAN; OSMOREGULATION; PRIORITY JOURNAL; REVIEW; TISSUE INJURY;

ACETAMINOPHEN; ANIMALS; CALPAIN; CELL DEATH; DISEASE PROGRESSION; FREE RADICALS; HUMANS; SOFT TISSUE INJURIES;

EID: 84859440714     PISSN: 01656147     EISSN: 18733735     Source Type: Journal    
DOI: 10.1016/j.tips.2012.01.003     Document Type: Review

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