RESUMO
Prolonged exposure to hexacarbon compounds is neurotoxic to humans and animals. As various hexacarbon compounds inhibit glycolytic enzymes in vitro, it has been suggested that this may underlie their neurotoxic effects in vivo. In the present investigation we examined whether long-term treatment with 2,5-hexanedione (200 mg/kg,sc) for 40 days affects the specific activity of brain and liver enolase, lactic dehydrogenase and malate dehydrogenase in female Wistar rats (150-170 g). Glycemia and liver glycogen levels were also determined. The specific activity of all enzymes tested, liver glycogen content and glycemia were not affected by chronic treatment with 2,5-hexanedione. Rats treated with 2,5-hexanedione weighed significantly less than control rats starting on day 18 of treatment (183 +/- 3.4 g for the vehicle group vs 171 +/- 3.2 g for the 2,5-hexanedione group). 2,5-Hexanedione also increased water intake (46% when compared to vehicle-treated rats). Prolonged treatment of rats with the non-neurotoxic hexacarbon 1,6-hexanediol (207 mg/kg, sc) significantly increased liver glycogen content (5.9 +/- 0.6 g/100 g for the vehicle group vs 9.0 +/- 1.1 g/100 g for the 1,6-hexanediol group) as well as food intake (44.0 +/- 1.5 g 100 g-1 6 days-1 for the vehicle vs 50.0 +/- 1.1 g 100 g-1 6 days-1 for the 1,6-hexanediol group).(ABSTRACT TRUNCATED AT 250 WORDS)
Assuntos
Encéfalo/enzimologia , Glicólise , Hexanonas/farmacologia , L-Lactato Desidrogenase/metabolismo , Fígado/enzimologia , Malato Desidrogenase/metabolismo , Fosfopiruvato Hidratase/metabolismo , Animais , Glicemia/análise , Peso Corporal , Hexanonas/metabolismo , Glicogênio Hepático/análise , Ratos , Ratos Endogâmicos , Fatores de TempoRESUMO
Prolonged exposure to hexacarbon compounds is neurotoxic to humans and animals. As various hexacarbon compounds inhibit glycolytic enzymes in vitro, it has been suggested that this may underlie their neurotoxic effects in vivo. in the present investigation we examined whether long-term treatment with 2,5-hexanedione (200 mg/kg, sc) for 40 days affects the specific activity of brain and liver enolase, lactic dehydrogenase and malate dehydrogenase in female Wistar rats (150-170 g). Glycemia and liver glycogen levels were also determined. The specific activity of all enzymes tested, liver glycogen content and glycemia were not affected by chronic treatment with 2,5-hexanedione. Rats treated with 2,5-hexanedione weighed significantly less than control rats starting on day 18 of treatment (183 ñ 3.4G for the vehicle groups vs 171 ñ 3.2G for the 2,5-hexanedione group). 2,5-hexanedione also increased water intake (46 por cento when compared to vehicle-treated rats). prolonged treatmentof rats with the non-neurotoxic hexacarbon 1,6-hexanediol (207 mg/kg, sc) significantly increased liver glycogen content (5.9 ñ 0.6g/100g for the vehicle group vs 9.0 ñ 1.1g/100 g for the 1.6-hexanediol group) as well as food intake (44.0 ñ 1.5g 100g-1 6 days-1 for thge 1,6-hexanediol group). These results indicate that long-term treatment with 2,5-hexanedione did not alter the brain and liver glycolytic enzymes studied, liver glycogen content or glycemia but did reduce weight gain and increased water intake, whereas the administration of the reportedly non-neurotoxic hexacarbon 1,6-hexanediol has demonstrable metabolic effects