Dynamics of pentavalent inorganic arsenic effects on some glycolytic and mitochondrial energy metabolizing enzymes in male Wistar rats

John Olabode Fatoki,Israel A Alabi,Tope G Atere,N.O Ibrahim,E.A Onifade,O.F Ojokuku,M.A Abdulateef,O.A Abisoye,P.K Raji,A Adeniyi,D.F Ademuyiwa,Comfort O Fatoki,Emmanuel B Oyewo,Jelili A Badmus

doi:10.1016/j.hazadv.2022.100111

Abstract

Exposure to environmental toxicants such as arsenic presents serious health challenges to humans. The effects of arsenic have been extensively evaluated, but there is a dearth of scientific findings on its effects on some key enzymes of glycolysis, Krebs cycle, and electron transport chain. This study, therefore, is aimed at investigating the time-course effects of arsenic exposure on these key enzymes in male Wistar rats. Rats (n = 45) were exposed to arsenic (100, 150, and 200 ppm) for 4, 8, and 12 weeks respectively in their drinking water. Control rats (n = 5) received drinking water for 12 weeks, after which blood and liver were removed from the animals and analyzed for some energy metabolizing enzymes spectrophotometrically. Data were analyzed using one-way analysis of variance followed by Tukey's post hoc test and p < 0.05 was considered significant. Our findings showed that arsenic exposure reduced the activities of plasma hexokinase at weeks 4, 8, and 12. Meanwhile, erythrocyte and liver homogenate hexokinase were significantly (p < 0.05) enhanced only at week 4. Plasma and liver aldolase activities were significantly (p < 0.05) induced at week 4, while aldolase activities of other compartments were significantly (p < 0.05) reduced at weeks 4, 8, and 12. In addition, arsenic significantly (p < 0.05) increased the activity of lactate dehydrogenase in various tissue compartments, effects of arsenic exposure were characterized by a significant (p < 0.05) decrease in the activities of malate dehydrogenase, complexes of the electron transport chain when compared with the control animals in all the tissues. These findings indicated that arsenic exposure induced various compartment-specific modulation of key enzymes of glycolysis, Krebs cycle and electron transport chain. This might be one of the mechanisms through which arsenic mediates its toxicity and its associated disease endpoints.

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