%0 Journal Article
%T Differential Expression ESTs Associated with Fluorosis in Rats Liver
%A Y. Q. He
%A Y. Pan
%A L. J. Ying
%A R. Zhao
%J International Journal of Genomics
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/208390
%X The fluoride has volcanic activity and abundantly exists in environment combining with other elements as fluoride compounds. Recent researches indicated that the molecular mechanisms of intracellular fluoride toxicity were very complex. However, the molecular mechanisms underlying the effects on gene expression of chronic fluoride-induced damage is unknown, especially the detailed regulatory process of mitochondria. In the present study, we screened the differential expression ESTs associated with fluorosis by DDRT-PCR in rat liver. We gained 8 genes, 3 new ESTs, and 1 unknown function sequence and firstly demonstrated that microsomal glutathione S-transferase 1 (MGST1), ATP synthase H+ transporting mitochondrial F0 complex subunit C1, selenoprotein S, mitochondrial IF1 protein, and mitochondrial succinyl-CoA synthetase alpha subunit were participated in mitochondria metabolism, functional and structural damage process caused by chronic fluorosis. This information will be very helpful for understanding the molecular mechanisms of fluorosis. 1. Introduction The fluoride has volcanic activity and abundantly exists in environment combining with other elements as fluoride compounds. With the development of the world economy, more and more organofluorine compounds are increasingly used. These compounds have a wide range of functions and can serve as agrochemicals, pharmaceuticals, refrigerants, pesticides, surfactants, fire-extinguishing agents, fibers, membranes, ozone depletors, and insulating materials [1, 2]. At the same time, in last decade, the fluoride effects have resurfaced due to the awareness that this element interacts with cellular systems even at low doses. Excessive fluoride intake over a long period of time may result in a serious public health problem called fluorosis, which is characterized by dental mottling and skeletal manifestations such as crippling deformities, osteoporosis, and osteosclerosis [3]. In recent years, metabolic, functional, and structural damage caused by chronic fluorosis have been reported in many tissues. Fluoride can induce oxidative stress and modulate intracellular redox homeostasis, lipid peroxidation, and protein carbonyl content, as well as alter gene expression and cause apoptosis. Genes modulated by fluoride include those related to the stress response metabolic enzymes, the cell-cell communications, and signal transduction [1]. In most cases, fluoride acts as an enzyme inhibitor, but fluoride ions can occasionally stimulate enzyme activity. Research data strongly suggest that fluoride inhibits protein
%U http://www.hindawi.com/journals/ijg/2012/208390/