[Heavy metal poisoning in relation to glucose-6-phosphate dehydrogenase activity in sheep erythrocytes]

Peroxidative lesions of cells and production of free radicals from endo- and exogenous reasons, eg. due to air pollution, can result in severe lesions of cells and subsequent pathological processes (Rieger, 1992; Robbins and Cotran, 1988). A pentose cycle plays an important role in the system of antioxidative protection: glucose-6-phosphate dehydrogenase (G-6-PD; EC 1.1.1.49) is its first enzyme. G-6-PD activity was evaluated in the erythrocytes of sheep kept in the region contaminated by heavy metals with mercury dominating among them, and in the same animals after administration of a feed mixture containing Hg, Pb Cd, Zn Cr, Cu, Fe and As (Fig. 1). Boehringer Mannheim test was used to determine the G-6-PD activity. There was no significant differences in the enzyme activity in the sheep from a contaminated region and in the animals outside the air-pollution region (control animals) before the applications of heavy metals started. The average value of G-6-PD activity was 13.96 +/- 0.94 mU.10 (-9) Ec in control animals and 14.39 +/- 1.49 mU.10 (-9) Ec in the animals from a contaminated region. After eight-day applications of heavy metals the G-6-PD activity increased statistically significantly to 18.71 +/- 2.45 mU.10 (-9) Ec; P < 0.01, and to 23.55 +/- 1.87 mU 10 (-9) Ec after 16 days of application; P < 0.001 (Fig. 2). An increase in G-6-PD activity after heavy metal applications is probably a compensation mechanism in the system of erythrocyte antioxidative protection due to higher peroxidation. The long term increased intake of heavy metals from polluted air did not lead to any rise of G-6-PD activity probably due to the lower dose of heavy metals and/or to adaptation of animal organisms to long run emission exposure. The results demonstrate that G-6-PD can be one of the biochemical indicators at organism load by heavy metals with mercury dominating among them.