Many results show that hydroquinone has a wide range of genotoxicity, it can lead to chromosomal aberrations, sister chromatid exchange (SCE), DNA-protein cross-links, DPC, DNA-DNA cross-linking, DNA strand breakage and so on.
Chromosomal Damage
Syrian hamster V79 cells in vitro toxicological test results show that hydroquinone (CAS NO: 123-31-9) can cause cell mutations, chromosomal aberrations, sister chromatid exchange and induce cell transformation.
It was reported, hydroquinone treatment can occur chromosomal aneuploidy, polyploidy, chromosomal deletions, sister chromatid exchange and other effects. Zhang L, etc. found that the use of fluorescence in situ hybridization, hydroquinone induced human lymphocytes 5 and 7 chromosome4q, causing HL60 cells on the 7th and the 9th chromosome aneuploidy effect.
Eastmond and other human lymphocytes treated with hydroquinone also appeared similar phenomenon, and found in the bone marrow pluripotent hematopoietic stem cells, CD34 + cells compared with CD34-cells are more sensitive to hydroquinone, and in human CD34 + CD19-cells in the bone marrow , hydroquinone induced selective deletion of chromosome 7 and 5q31, no effect on chromosome 8. Because of persistent structural chromosome abnormalities and number of leukemia cases in humans are often observed, therefore, hydroquinone chromosome damaging effects of its cause bone marrow or blood abnormalities of internal factors.
DNA Damage
Hydroquinone can be damaged by a variety of ways DNA. It has been reported, under neutral conditions hydroquinone spontaneously oxidized to produce superoxide anion, and a quinone compound semiquinone.
Superoxide anion can lead to hydrogen peroxide (H2O2) and hydroxyl radicals (• OH) radical chain reaction, and into the cells, the DNA formed near • OH; superoxide anion can be protonated, across the membrane and DNA near • OH produced H2O2, produce oxidative damage to DNA.
Ceusilva such as hydroquinone exposure with V79 cells, oxidative DNA damage was detected reflect the characteristic Indicator 8 – hydroxy – base guanine (8-OH-G) content. The results show that they have significantly increased trend. 8-OH-G can cause mutations that induce DNA strand breaks, and has been reported with its content micronucleus formation has some relevance. Another mechanism of DNA damage may be due to the oxidation of hydroquinone product inhibition of DNA topoisomerase II activity, Leu et al found that the oxidation products of hydroquinone, 1,4 – benzoquinone and 4,4 ‘- benzoquinone can inhibit the DNA chain on protein–topoisomerase II. DNA-topoisomerase II is an SH group-dependent endonucleases, DNA topoisomerase II by cleavage of the purine / pyrimidine repeat sequences involved in DNA replication, recombination, and structural maintenance of chromosome segregation. Once topoisomerase II is destroyed, will lead to DNA helicase, releasing DNA circles (100p), causes DNA strand breaks, DNA strand breaks may induce DNA strand inappropriate regrouping exception occurred mitotic recombination, abnormal restructuring will lead to cell death or chromosomal mutations.
DNA damage and genetic structure of the abnormal and the resulting expression of oncogenes and tumor suppressor genes or functional changes in cell mutations and malignant transformation is a prerequisite.
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