Influence of acidosis and lactate on protein degradation in adult and fetal hearts

• Published in: Journal of molecular and cellular cardiology Vol. 12; no. 10; pp. 1065 - 1074
• Main Authors: Crie, J.Stanley, Wildenthal, Kern
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.10.1980
• Subjects: Acidosis - metabolism; Alanine; Alanine - metabolism; Amino Acids - metabolism; Amino Acids, Branched-Chain - metabolism; Animals; Branched-chain amino acids; Female; Heart - embryology; Lactates - pharmacology; Lactic acidosis; Male; Mice; Myocardium - metabolism; Organ Culture Techniques; Perfusion; Phenylalanine - metabolism; Pregnancy; Protein degradation; Proteins - metabolism; Rats; Taurine; Taurine; Protein degradation; Alanine; Branched-chain amino acids; Lactic acidosis
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1016/0022-2828(80)90032-2

The influence of lactic acidosis, lactate alone, and acidosis alone on proteolysis and amino acid release of adult and fetal hearts was investigated in adult rat hearts and fetal mouse hearts. Phenylalanine release in the presence of cycloheximide was used as an index of protein degradation. Proteolysis in fetal hearts was not altered by lactate or acidosis, either singly or combined. In contrast, adult hearts were highly sensitive to lactic acidosis; lactate (15 m m) at pH 6.8 caused a 67% decrease in phenylalanine release, from 0.15 ± 0.004 to 0.05 ± 0.005 nmol (mg heart wt) −1 h −1. Lactate (15 m m) at neutral pH did not alter the rate of protein degradation of perfused rat hearts, whereas CO 2-induced acidosis (pH 6.8) reduced phenylalanine release by 27% ( P < 0.01). Alanine release, relative to that of phenylalanine, was stimulated by lactate and lactic acidosis in both adult and fetal hearts, presumably as a result of increased alanine synthesis from pyruvate. Release of the branched-chain amino acids was reduced by lactate in adult hearts but was increased in fetal hearts. Taurine release was increased 133% from hearts perfused in the presence of lactic acidosis but was not increased in fetal hearts.