Is lead toxicosis a reflection of altered energy metabolism in brain synaptosomes?
The aim of the experiments presented here was to discern whether prolonged consumption of leaden water, that imitates environmental exposure, affects some energetic parameters in nerve endings of adult rat brains. Our results indicated that during chronic lead intoxication the oxidation chain of synaptic mitochondria remains intact. The oxygen consumption by synaptosomes and activity of cytochrom oxidase in synaptic and pericarionic mitochondria obtained from intoxicated rats did not change in comparison to those from the control samples. Compared with the control samples, the concentration of ATP decreased and the concentration of creatine phosphate (CrP) increased drastically in fractions obtained from Pb2+ intoxicated animals with simultaneously increased activity of creatine kinase (CK). It seems likely that, the CrP/Cr/CK system constitutes a satisfactory regulatory mechanism for chronic Pb2+ toxicity effects on energy metabolism in nerve endings of the adult rats.
Rafałowska
U
U
Department of Neurochemistry, Polish Academy of Sciences, Warsaw, Poland.
Struzyńska
L
L
Dabrowska-Bouta
B
B
Lenkiewicz
A
A
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D003402:Creatine Kinase / Q000378:metabolism; D004734:Energy Metabolism; D007855:Lead Poisoning / Q000378:metabolism*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013574:Synaptosomes / Q000378:metabolism*
D000255:Adenosine Triphosphate; D003402:Creatine Kinase