Karthikeyan J, Bavani G
Department of Biotechnology, D.G. Vaishnav College, Arumbakkam, Chennai 600 106, India.
J Environ Biol. 2009 Sep;30(5 Suppl):895-8.
Cadmium is known to be an environmental and industrial pollutant. Exposure to cadmium is known to affect various tissues. The purpose of this study is to determine the toxic effects of cadmium on lactate dehydrogenase (LDH) isoenzymes. Administration of cadmium chloride (3 mg kg(-1)) resulted in the reduction of LDH4 fraction of liver tissue indicating the inhibitory effect of cadmium. The LDH1 LDH3 and LDH5 fractions showed decreasing trend initially but there was a significant increase later In contrast the LDH2 fraction showed increasing trend after 24 hr from the last dosage it was elevated after 30 days. The total activity of LDH in liver showed gradual reduction in both groups. The activity of succinate dehydrogenase (SDH) the mitochondrial enzyme has been observed to be inhibited by cadmium with the possibility of interfering with energy transport mechanism. Na(+)- K(+)-ATPase activity of liver also showed similar decrease after cadmium administration which may lead to general deficit in cell membrane transport. As cadmium shows drastic decrease in all the enzymes studied, the LDH2 fraction which sharply rises from the control may be used as a marker enzyme to asses the liver injury.
已知镉是一种环境和工业污染物。已知接触镉会影响多种组织。本研究的目的是确定镉对乳酸脱氢酶（LDH）同工酶的毒性作用。给予氯化镉（3 mg kg⁻¹）导致肝脏组织中LDH4组分减少，表明镉具有抑制作用。LDH1、LDH3和LDH5组分最初呈下降趋势，但后来显著增加。相比之下，LDH2组分在最后一次给药24小时后呈上升趋势，30天后升高。两组肝脏中LDH的总活性均逐渐降低。已观察到线粒体酶琥珀酸脱氢酶（SDH）的活性受到镉的抑制，可能会干扰能量转运机制。镉给药后肝脏的Na⁺-K⁺-ATP酶活性也出现类似下降，这可能导致细胞膜转运普遍不足。由于镉使所有研究的酶都大幅下降，从对照组急剧上升的LDH2组分可作为评估肝损伤的标记酶。
