Abstract
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.
Highlights
The fluoride has volcanic activity and abundantly exists in environment combining with other elements as fluoride compounds
Research data strongly suggest that fluoride inhibits protein secretion and/or synthesis and that it influences distinct signaling pathways involved in proliferation and apoptosis including the mitogen-activated protein kinase (MAPK), p53, activator protein-1 (AP-1), and nuclear factor kappa B (NF-κB) pathways [4,5,6]
According to the results of the sequence BLAST, we gained 8 genes, 3 new expressed sequence tags (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 succinylCoA synthetase alpha subunit were participated in mitochondria metabolism, functional and structural damage process caused by chronic fluorosis
Summary
The fluoride has volcanic activity and abundantly exists in environment combining with other elements as fluoride compounds. 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. Information about the molecular mechanism of fluoride-induced tissue damage is almost unknown. Fluoride alters the activity of many mitochondria-rich cells such as those of the human kidney and the rat liver [8, 9], but the molecular mechanisms of chronic fluoride-induced mitochondrial damage are scarce. In order to Comparative and Functional Genomics get a deeper understanding of the molecular mechanisms underlying the effects of fluoride on mitochondrial gene expression and metabolism, we screened differential display genes or expressed sequence tags (ESTs) involved in SpragueDawley rats with fluorosis
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