Abstract
The effects of cadmium (Cd) on the enzymatic activities of glucose 6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD) were investigated in the gill, liver and kidney tissues of rainbow trout (Oncorhynchus mykiss). Three test groups of fish were subjected to increasing concentrations (1, 3 and 5 mg/l) of cadmium (Cd) in vivo, respectively. The G6PD and 6PGD activities in the gill, liver, and kidney tissues of each group of fish were measured on days 1, 3, 5 and 7. G6PD and 6PGD enzyme activities, measured in gill, liver and kidney homogenates, were stimulated by various concentrations (1, 3, and 5 mg/l) of cadmium. Although the dose-response pattern of G6PD enzyme activities in liver and kidney tissue was very similar, that in gill was different from both other tissues. The enzyme activity of G6PD enzyme was significantly stimulated after three days (Day 3) in liver and kidney tissues at a dose of 1 mg/l Cd (p < 0.05), whereas it was stimulated on the first day of experiment (Day 1) in gill, liver and kidney tissues at doses of 3 and 5 mg/l Cd (p < 0.05). However, the activity of 6PGD was stimulated after three days (Day 3) in the liver at a dose of 1 mg/l Cd (p < 0.05) and on the first day in gill, liver and kidney tissues at doses of 3 and 5 mg/l Cd (p < 0.05). The stimulation effect of the 5 mg/l dose of Cd on G6PD and 6PGD enzyme activities was significantly diminished after seven days (Day 7) in all tissues (p < 0.05). In contrast to the dose-response pattern at the dose of 5 mg/l Cd, G6PD and 6PGD enzyme activities were stimulated significantly (p < 0.05) in liver and kidney tissues at the doses of 3 and 1 mg/l Cd. The stimulation effect of cadmium on the three tissues studied was also calculated; for both of the enzymes (G6PD and 6PGD), the enzyme activity levels were stimulated by approximately 60% and 38% in gills, 68% and 44% in liver, and 67% and 41% in kidneys, respectively, over the base-line enzyme activity of the control groups during the sevenday experimental period. These findings indicate that tissue G6PD and 6PGD enzymes function to protect against cadmium toxicity.
Highlights
glucose 6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD) enzyme activities, measured in gill, liver and kidney homogenates, were stimulated by various concentrations (1, 3, and 5 mg/l) of cadmium
It is generally recognized that the cell has four major NADPH-production systems that correspond to the activities of four cytoplasmatic enzymes: glucose 6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD) belong to the pentose phosphate pathway, malic enzyme (ME) and NADP-dependent isocitrate dehydrogenase (NADP-IDH)
The specific enzyme activity of G6PD and 6PGD in kidney, liver, and gill tissue of rainbow trout exposed to three different concentrations of cadmium (1, 3, and 5 mg/l Cd) were measured on days 1, 3, 5 and 7
Summary
G6PD and 6PGD enzyme activities, measured in gill, liver and kidney homogenates, were stimulated by various concentrations (1, 3, and 5 mg/l) of cadmium. In contrast to the dose-response pattern at the dose of 5 mg/l Cd, G6PD and 6PGD enzyme activities were stimulated significantly (p < 0.05) in liver and kidney tissues at the doses of 3 and 1 mg/l Cd. The stimulation effect of cadmium on the three tissues studied was calculated; for both of the enzymes (G6PD and 6PGD), the enzyme activity levels were stimulated by approximately 60% and 38% in gills, 68% and 44% in liver, and 67% and 41% in kidneys, respectively, over the base-line enzyme activity of the control groups during the sevenday experimental period. The stimulation effect of cadmium on the three tissues studied was calculated; for both of the enzymes (G6PD and 6PGD), the enzyme activity levels were stimulated by approximately 60% and 38% in gills, 68% and 44% in liver, and 67% and 41% in kidneys, respectively, over the base-line enzyme activity of the control groups during the sevenday experimental period These findings indicate that tissue G6PD and 6PGD enzymes function to protect against cadmium toxicity. Like the other heavy metals such as mercury and lead, cadmium causes significant metabolic alterations, e.g. enzymatic activities and membrane transport mechanisms (Viarengo 1989) and injuries of biological systems at different levels (Pratap and Wendelaar-Bonga 1990)
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