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- W1964180520 abstract "The site and mode of action of acrylamide (ACR), γ-diketone hexacarbons and 3,3′-iminodipropionitrile (IDPN) in producing a neurofilamentous axonopathy are unknown. Whether the neuropathy is caused by reductions in axonal transport produced by energy depletion is under investigation. Reductions in the quantity of proteins fast transported following a single dose of ACR or neurotoxic γ-diketones have been reported25,26. The current study examines the in vitro effects of these toxicants upon ATP production by mitochondria. Isolated rat brain mitochondria incubated for 30 min at 37°C with neurotoxic doses of ACR (0.7 mM) or 3,4-dimethyl-2,5-hexanedione (0.25 mM) retained similar capacities for synthesis of ATP from pyruvate and endogenous concentrations of ATP compared to controls. 2,5-Hexanedione (2,5-HD; 4 mM) and IDPN (0.1%) significantly reduced the rate of synthesis (−22.5% and −15%, respectively); but only 2,5-HD decreased the endogenous concentration of ATP (−21.6%) following a single 30 min exposure. Toxicant action on ATP production is limited to 2,5-HD; the lack of correlation between the toxicant-induced changes in axonal transport and mitochondrial ATP production demonstrate the necessity to evaluate other structures as the critical site of action in producing axonal transport changes." @default.
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- W1964180520 date "1990-09-01" @default.
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- W1964180520 title "Effects of neurofilamentous axonopathy-producing neurotoxicants on in vitro production of ATP by brain mitochondria" @default.
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- W1964180520 doi "https://doi.org/10.1016/0006-8993(90)90190-m" @default.
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