Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.5.1.2 (DNA ligase)
 2,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The oxidation of DNA and lipid was analysed in the marine mussel (Mytilus edulis) in response to exposure (10microg/l and 200microg/l) to cadmium (Cd) and chromium [Cr(VI)]. Concentration dependent uptake of both metals into mussel tissues was established and levels of gill ATP were not depleted at these exposure levels. DNA strand breakage in gill cells (analysed by the comet assay) was elevated by both metals, however, DNA oxidation [measured by DNA strand breakage induced by the DNA repair enzyme formamidopyrimidine glycosylase (FPG)] was not elevated. This was despite a statistically significant increase in both malondialdehyde and 4-hydroxynonenal - indicative of lipid peroxidation - following treatment with Cd. In contrast, both frank DNA stand breaks and FPG-induced DNA strand breaks (indicative of DNA oxidation) were increased following injection of mussels with sodium dichromate (10.4microgCr(VI)/mussel). The metals also showed differential inhibitory potential towards DNA repair enzyme activity with Cd exhibiting inhibition of DNA cutting activity towards an oligonucleotide containing 8-oxo-7,8-dihydro-2'-deoxyguanosine and Cr(VI) showing inhibition of such activity towards an oligonucleotide containing ethenoadenosine, both at 200microg/l. The metals thus show DNA damage activity in mussel gill with distinct mechanisms involving both direct and indirect (oxidative) DNA damage, as well as impairing different DNA repair capacities. A combination of these activities can contribute to adverse effects in these organisms.
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PMID:Macromolecule oxidation and DNA repair in mussel (Mytilus edulis L.) gill following exposure to Cd and Cr(VI). 1733 96

Occupational exposure to Cr (VI) can cause DNA damage, genetic instability and elevate the risk of cancer. Here we investigated Cr (VI)-induced DNA damage and 8-oxoguanine DNA glycosylase 1 (hOGG1) gene expression in electroplating workers. The hOGG1 gene encodes a DNA repair enzyme that is crucial in DNA oxidation damage repair. Deficiency in hOGG1 DNA repair capacity contributes to the accumulation of DNA damage and genetic instability. To address the issues, we collected peripheral blood samples and urine samples from 162 electroplating workers and 84 control subjects. We measured blood chromium levels, urine chromium levels, DNA damage, and hOGG1 mRNA expression. We found significantly higher levels of blood chromium, urine chromium, and DNA damage in electroplating workers compared with controls, whereas mRNA levels of the hOGG1 gene were significantly lower in the exposed workers. Furthermore, in electroplating workers we found that blood Cr had a positive association with DNA damage as measured with the tail DNA%. Meanwhile, tail DNA% was positively associated with hOGG1 mRNA expression. Finally, the effect of potassium dichromate treatment was investigated in a human B lymphoblastoid cell line (LCL). We observed that potassium dichromate induced a concentration-dependent decrease in hOGG1 mRNA. After removing the K2Cr2O7-containing medium for 3 days and 7 days, the abundance of hOGG1 mRNA expression recovered to a similar level as the controls. Collectively, our findings suggest that decreased hOGG1 mRNA expression in occupationally exposed populations partially contribute to Cr (VI) induced DNA damage.
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PMID:Decreased 8-oxoguanine DNA glycosylase 1 (hOGG1) expression and DNA oxidation damage induced by Cr (VI). 3049 37