[Antioxidant enzymes, hydrogen peroxide metabolism, and respiration in rat heart during experimental hyperammonemia].
The effects of toxic ammonia doses on H2O2 metabolism, energy metabolism, and antioxidant enzyme activities in rat heart were studied. Ammonium acetate administration to animals proved to increase total superoxide dismutase (SOD), catalase, and glutathione peroxidase activities in the heart cytoplasmic fraction as well as Mn-SOD, catalase, and glutathione reductase in heart mitochondria. Conversely, ammonia inhibited the same activities in the brain, liver, and erythrocytes. Hyperammonemia had no effect on the levels of ATP, ADP and total adenine nucleotides in the heart but decreased them in the brain. Ammonia impaired oxidative phosphorylation and increased the rate of H202 production in heart and brain mitochondria. The ammonia concentration inhibiting antioxidant enzymes in the liver and brain can be insufficient for such effect in the heart.
Venediktova
N I
NI
Kosenko
E A
EA
Kaminskiĭ
Iu G
IuG
D000085:Acetates / Q000008:administration & dosage / Q000633:toxicity; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001921:Brain / Q000201:enzymology; D001923:Brain Chemistry / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000378:metabolism*; D022124:Hyperammonemia / Q000139:chemically induced / Q000201:enzymology* / Q000503:physiopathology; D008099:Liver / Q000201:enzymology; D008297:Male; D009206:Myocardium / Q000201:enzymology*; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010088:Oxidoreductases / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar
D000085:Acetates; D000975:Antioxidants; D006861:Hydrogen Peroxide; D010088:Oxidoreductases; C018824:ammonium acetate