Biochemical aspects of fluoroacetate poisoning in isolated rat kidney tubules: reversibility of inhibition of gluconeogenesis by alpha-ketoglutarate.
The effects of monofluoroacetate (FAC) on suspensions of isolated rat kidney tubules were investigated. FAC inhibited gluconeogenesis from lactate, pyruvate, fructose, dihydroxyacetone, alpha-ketoglutarate, and succinate. The gluconeogenesis from pyruvate, ketoglutarate, and lactate was less sensitive to FAC than that from other substrates. FAC also caused a decrease in oxygen consumption, hydroxybutyrate to acetoacetate ratio, alpha-ketoglutarate, ATP, and total adenine nucleotide content; the citrate content was increased. Addition of alpha-ketoglutarate, 5 mmol/l, caused a reversal of gluconeogenesis inhibition, an increase in ATP content, and a delay in citrate accumulation in isolated rat kidney tubules incubated with FAC.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002951:Citrates / Q000378:metabolism; D005463:Fluoroacetates / Q000037:antagonists & inhibitors / Q000506:poisoning*; D005632:Fructose / Q000378:metabolism; D005943:Gluconeogenesis / Q000187:drug effects*; D066298:In Vitro Techniques; D007656:Ketoglutaric Acids / Q000494:pharmacology*; D007684:Kidney Tubules / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains
D002951:Citrates; D005463:Fluoroacetates; D007656:Ketoglutaric Acids; D005632:Fructose; D000255:Adenosine Triphosphate