Glucose-dependent lactate production by homogenates of neuronal tissues prepared from rats treated with 2,4-dithiobiuret, acrylamide, p-bromophenylacetylurea and 2,5-hexanedione

Richard M. LoPachin, R. W. Moore, L. A. Menahan, R. E. Peterson

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17 Citations (Scopus)

Abstract

Chronic treatment of rats with dithiobiuret (DTB) produces a delayed onset muscle weakness and, as suggested by a preliminary study, a distal axonopathy. An inhibition of glycolysis resulting in an energy deficit has been suggested as a possible mechanism of neurotoxin-induced distal axonopathies. To determine whether chronic DTB administration (1 mg/kg/day x 7 days; sacrificed on Day 7) might be associated with a perturbation of glucose metabolism in neuronal tissues, lactate production was measured in brain and spinal cord homogenates prepared from rats which exhibited hindlimb skeletal muscle weakness. Kinetic and statistical analysis showed that glucose-dependent lactate production in these homogenates was not different from that of controls. Lactate production was also determined in brain homogenates prepared from rats intoxicated with acrylamide (50 mg/kg/day x 9 days; sacrificed on Day 9), p-bromophenylacetylurea (200 mg/kg/day x 2 days; sacrified on Day 14) or 2,5-hexanedione (400 mg/kg/day x 21 days; sacrificed on Day 21). The results indicated that whereas 2,5-hexanedione produced a slight decrease in V(max), acrylamide and p-bromophenylacetylurea did not cause changes in glucose-dependent lactate production. These findings do not support the suggestion that an inhibition of glycolysis represents a common biochemical lesion associated with neurotoxins which cause delayed onset muscle weakness and distal axonopathy.

Original languageEnglish (US)
Pages (from-to)25-36
Number of pages12
JournalNeuroToxicology
Volume5
Issue number2
StatePublished - 1984
Externally publishedYes

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Acrylamide
Rats
Lactic Acid
Muscle Weakness
Tissue
Muscle
Glucose
Neurotoxins
Glycolysis
Brain
Hindlimb
Metabolism
Spinal Cord
Statistical methods
Skeletal Muscle
Kinetics
4-bromophenylacetylurea
2,5-hexanedione
2,4-dithiobiuret

ASJC Scopus subject areas

  • Neuroscience(all)
  • Cellular and Molecular Neuroscience
  • Toxicology

Cite this

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title = "Glucose-dependent lactate production by homogenates of neuronal tissues prepared from rats treated with 2,4-dithiobiuret, acrylamide, p-bromophenylacetylurea and 2,5-hexanedione",
abstract = "Chronic treatment of rats with dithiobiuret (DTB) produces a delayed onset muscle weakness and, as suggested by a preliminary study, a distal axonopathy. An inhibition of glycolysis resulting in an energy deficit has been suggested as a possible mechanism of neurotoxin-induced distal axonopathies. To determine whether chronic DTB administration (1 mg/kg/day x 7 days; sacrificed on Day 7) might be associated with a perturbation of glucose metabolism in neuronal tissues, lactate production was measured in brain and spinal cord homogenates prepared from rats which exhibited hindlimb skeletal muscle weakness. Kinetic and statistical analysis showed that glucose-dependent lactate production in these homogenates was not different from that of controls. Lactate production was also determined in brain homogenates prepared from rats intoxicated with acrylamide (50 mg/kg/day x 9 days; sacrificed on Day 9), p-bromophenylacetylurea (200 mg/kg/day x 2 days; sacrified on Day 14) or 2,5-hexanedione (400 mg/kg/day x 21 days; sacrificed on Day 21). The results indicated that whereas 2,5-hexanedione produced a slight decrease in V(max), acrylamide and p-bromophenylacetylurea did not cause changes in glucose-dependent lactate production. These findings do not support the suggestion that an inhibition of glycolysis represents a common biochemical lesion associated with neurotoxins which cause delayed onset muscle weakness and distal axonopathy.",
author = "LoPachin, {Richard M.} and Moore, {R. W.} and Menahan, {L. A.} and Peterson, {R. E.}",
year = "1984",
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T1 - Glucose-dependent lactate production by homogenates of neuronal tissues prepared from rats treated with 2,4-dithiobiuret, acrylamide, p-bromophenylacetylurea and 2,5-hexanedione

AU - LoPachin, Richard M.

AU - Moore, R. W.

AU - Menahan, L. A.

AU - Peterson, R. E.

PY - 1984

Y1 - 1984

N2 - Chronic treatment of rats with dithiobiuret (DTB) produces a delayed onset muscle weakness and, as suggested by a preliminary study, a distal axonopathy. An inhibition of glycolysis resulting in an energy deficit has been suggested as a possible mechanism of neurotoxin-induced distal axonopathies. To determine whether chronic DTB administration (1 mg/kg/day x 7 days; sacrificed on Day 7) might be associated with a perturbation of glucose metabolism in neuronal tissues, lactate production was measured in brain and spinal cord homogenates prepared from rats which exhibited hindlimb skeletal muscle weakness. Kinetic and statistical analysis showed that glucose-dependent lactate production in these homogenates was not different from that of controls. Lactate production was also determined in brain homogenates prepared from rats intoxicated with acrylamide (50 mg/kg/day x 9 days; sacrificed on Day 9), p-bromophenylacetylurea (200 mg/kg/day x 2 days; sacrified on Day 14) or 2,5-hexanedione (400 mg/kg/day x 21 days; sacrificed on Day 21). The results indicated that whereas 2,5-hexanedione produced a slight decrease in V(max), acrylamide and p-bromophenylacetylurea did not cause changes in glucose-dependent lactate production. These findings do not support the suggestion that an inhibition of glycolysis represents a common biochemical lesion associated with neurotoxins which cause delayed onset muscle weakness and distal axonopathy.

AB - Chronic treatment of rats with dithiobiuret (DTB) produces a delayed onset muscle weakness and, as suggested by a preliminary study, a distal axonopathy. An inhibition of glycolysis resulting in an energy deficit has been suggested as a possible mechanism of neurotoxin-induced distal axonopathies. To determine whether chronic DTB administration (1 mg/kg/day x 7 days; sacrificed on Day 7) might be associated with a perturbation of glucose metabolism in neuronal tissues, lactate production was measured in brain and spinal cord homogenates prepared from rats which exhibited hindlimb skeletal muscle weakness. Kinetic and statistical analysis showed that glucose-dependent lactate production in these homogenates was not different from that of controls. Lactate production was also determined in brain homogenates prepared from rats intoxicated with acrylamide (50 mg/kg/day x 9 days; sacrificed on Day 9), p-bromophenylacetylurea (200 mg/kg/day x 2 days; sacrified on Day 14) or 2,5-hexanedione (400 mg/kg/day x 21 days; sacrificed on Day 21). The results indicated that whereas 2,5-hexanedione produced a slight decrease in V(max), acrylamide and p-bromophenylacetylurea did not cause changes in glucose-dependent lactate production. These findings do not support the suggestion that an inhibition of glycolysis represents a common biochemical lesion associated with neurotoxins which cause delayed onset muscle weakness and distal axonopathy.

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