[Diabetes and calcium transportation in liver mitochondria]

It is a well known fact that isolated, energized mitochondria take up large amounts of Ca2+, thus regulating their own internal Ca2+ concentration and modulating the activity of matrix dehydrogenases involved in the aerobic steps of glucose oxidation. The information available on biochemical alterations in diabetes is extensive but no data on Ca2+ transport alterations have been reported. Therefore, it seemed of interest to study Ca2+ uptake and release (efflux) by liver mitochondria of diabetic rats, in relation to other metabolic parameters representing the energization state of the inner mitochondrial membrane. Rats (male; 200 +/- 20 g body weight) were injected with streptozotocin (65 mg/kg) and after 1-3 months, liver mitochondria were isolated and suspended in an isotonic medium supplemented with 3.0 microM rotenon, 5.0 mM succinate (the energy source), 50 microM Antipyrylazo III and CaCl2 (20-100 microM Ca2+). Ca2+ uptake was monitored by the decrease of the Ca2(+)-Antipyrylazo III complex concentration, measured spectrophotometrically at 720-790 nm and 30 degrees C. The initial rates of Ca2+ uptake (in nmol Ca2+/min/mg of protein; average +/- S.E., n = 5) were as follows (in parenthesis, initial [Ca2+] microM): normal mitochondria, 171 +/- 20 (20); 207 +/- 13 (40); 233 +/- 22 (60) and 237 +/- 14 (100); diabetic mitochondria, 114 +/- 13; 134 +/- 22; 186 +/- 7 and 184 +/- 14, respectively. Accordingly, the decrease of Ca2+ uptake activity was 33, 36, 20 and 22 (%), respectively (P less than 0.05 at all [Ca2+].(ABSTRACT TRUNCATED AT 250 WORDS)