Skowerski M, Jasik K, Konecki J
2nd Clinic of Cardiology, Silesian Medical University, ul. Ziolowa 47, 40-635 Katowice, Poland.
Med Sci Monit. 2000 Mar-Apr;6(2):258-65.
Heavy metals tend to occur in increasingly many aspects of human activities. Studies of cadmium (Cd) have revealed that it is extremely toxic in its effects. It is known that selenium (Se) may suppress deleterious effects of Cd. We investigated the effects of dietary Cd-intoxication on the incorporation of precursors of RNA, protein and ANP (atrial natriuretic peptide) granule synthesis in mouse cardiocytes and compared them with the results of Se interaction with Cd-intoxication. Functional condition of the heart was evaluated on the basis of the number of ANP granules synthesized in cardiocytes of the right atrium in the mice exposed to the tested elements. The experiment was conducted on 100 male white Balby mouse during the period of three months. The animals were divided into four groups. The control group I (C) was fed a standard Murigran diet. Group II (Cd)--received 50 ppm Cd as cadmium acetate in drinking water. Group III (Se) received a standard diet supplemented with 5.0 mg Se/kg DM/24 h as acid sodium selenate. The experimental animals in group IV (Cd + Se)--were fed a diet supplemented with Cd and Se in the same amounts as the above groups. Our results revealed that after 3 months long intoxication with Cd, 3H-uridine and 3H-alanine uptakes to cardiomyocytes were decreased by 33% and 40%, respectively, and fewer ANP granules were synthesized when compared with the controls. Ultrastructure of myocytes proved slightly distorted. Se-intoxicated cardiomyocytes indicated diminished incorporation of RNA synthesis precursors by 17% and 27% in the ventricle and atrium, respectively, in comparison with the controls. Some Se-induced structural changes were observed. Finally, after Se in interaction with Cd intoxication, the uptake of 3H-uridine and 3H-alanine to cardiocytes was higher and the number of ANP granules increased. The values approximated those in the controls. We concluded that: prolonged Cd intoxication disturbed intercellular metabolism by damaging ultrastructural elements and suppressing the incorporation of precursors of RNA, protein and ANP granule synthesis. Se in interaction with Cd revealed protective effects against Cd toxicity. After Cd-Se-intoxication neither metabolic activity nor cardiocyte ultrastructure showed significant differences from those in the controls.
重金属在人类活动的诸多方面愈发常见。对镉（Cd）的研究表明，其毒性极强。已知硒（Se）可抑制镉的有害作用。我们研究了膳食镉中毒对小鼠心肌细胞中RNA、蛋白质和心钠素（ANP）颗粒合成前体掺入的影响，并将其与硒与镉中毒相互作用的结果进行比较。根据暴露于受试元素的小鼠右心房心肌细胞中合成的心钠素颗粒数量，评估心脏的功能状态。实验在100只雄性白色Balby小鼠上进行，为期三个月。动物被分为四组。对照组I（C）喂食标准Murigran饲料。第二组（Cd）——在饮用水中摄入50 ppm的醋酸镉形式的镉。第三组（Se）接受补充有5.0 mg硒/千克干物质/24小时的亚硒酸钠的标准饲料。第四组（Cd + Se）的实验动物——喂食补充有与上述组相同数量的镉和硒的饲料。我们的结果显示，镉中毒3个月后，心肌细胞对3H-尿苷和3H-丙氨酸的摄取分别降低了33%和40%，与对照组相比，合成的心钠素颗粒更少。心肌细胞的超微结构显示略有扭曲。与对照组相比，硒中毒的心肌细胞在心室和心房中RNA合成前体的掺入分别减少了17%和27%。观察到一些硒诱导的结构变化。最后，在硒与镉中毒相互作用后，心肌细胞对3H-尿苷和3H-丙氨酸的摄取增加，心钠素颗粒数量增多。这些值接近对照组。我们得出结论：长期镉中毒通过破坏超微结构元件并抑制RNA、蛋白质和心钠素颗粒合成前体的掺入，扰乱细胞间代谢。硒与镉相互作用显示出对镉毒性的保护作用。镉 - 硒中毒后，代谢活性和心肌细胞超微结构与对照组相比均无显著差异。
