DNA damage by oxygen‐derived species Its mechanism and measurement in mammalian systems

Halliwell, Barry; Aruoma, Okezie I.

doi:10.1016/0014-5793(91)80347-6

Cited by 1,405 publications

(645 citation statements)

References 184 publications

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“…The in vitro culture environment differs from in vivo conditions in that the oxygen concentration is higher, and, in such a condition, mouse embryos show a higher ROS concentration in simple culture media (117,118). Reactive oxygen species are thought to cause damage to the cell membrane (119) and to cause DNA fragmentation in somatic cells (120), and they may participate in the process of apoptosis (121). Apoptotic configurations in fragmented human embryos were observed at a stage before blastocyst formation, and these have been suggested as the process of programmed cell death (122).…”

Section: Reactive Oxygen Species In Human Embryosmentioning

confidence: 99%

Role of reactive oxygen species in the pathophysiology of human reproduction

Agarwal

Saleh

Bedaiwy

2003

Fertility and Sterility

1,272

909

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Objective: To summarize the role of reactive oxygen species (ROS) in the pathophysiology of human reproduction. Design: Review of literature. Setting: Fertility research center and obstetrics and gynecology department in a tertiary care facility. Result(s): ROS plays an essential role in the pathogenesis of many reproductive processes. In male-factor infertility, oxidative stress attacks the fluidity of the sperm plasma membrane and the integrity of DNA in the sperm nucleus. Reactive oxygen species induced DNA damage may accelerate the process of germ cell apoptosis, leading to the decline in sperm counts associated with male infertility. ROS mediated female fertility disorders share many pathogenic similarities with the ones on the male side. These similarities include a potential role in the pathophysiology of endometriosis and unexplained infertility. High follicular fluid ROS levels are associated with negative IVF outcomes, particularly in smokers. Moreover, oxidative stress may be responsible in hydrosalpingeal fluid mediated embryotoxicity as well as poor in vitro embryonic development. Conclusion(s):High levels of ROS are detrimental to the fertility potential both in natural and assisted conception states. (Fertil Steril 2003;79:829 -43.

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Section: Reactive Oxygen Species In Human Embryosmentioning

confidence: 99%

Role of reactive oxygen species in the pathophysiology of human reproduction

Agarwal

Saleh

Bedaiwy

2003

Fertility and Sterility

1,272

909

View full text Add to dashboard Cite

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“…Reactive oxygen species (ROS) are generated through endogenous cellular oxygen metabolism and by exogenous environmental factors [1,2]. ROS react with DNA, RNA, and their precursors.…”

Section: Introductionmentioning

confidence: 99%

Effects of base excision repair proteins on mutagenesis by 8-oxo-7,8-dihydroguanine (8-hydroxyguanine) paired with cytosine and adenine

2010

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, also known as 8-hydroxyguanine) is a major base lesion that is generated by reactive oxygen species in both the DNA and nucleotide pool. The role of DNA glycosylases, which initiate base excision repair, in the mutagenic processes of 8-oxo-Gua in DNA and 8-oxo-7,8-dihydro-2'-deoxyguanosine 5'-triphosphate (8-oxo-dGTP, also known as 8-hydroxy-2'-deoxyguanosine 5'-triphosphate) were investigated using supF shuttle plasmids propagated in human cells. The DNA glycosylases, OGG1, MUTYH, NTH1, and NEIL1, in 293T cells were individually knocked-down by siRNAs and plasmid DNAs containing an 8-oxo-Gua:C/8-oxo-Gua:A pair, and 8-oxo-dGTP plus unmodified plasmid DNA were then introduced into the knocked-down cells. The knock-down of OGG1, MUTYH, NTH1, and NEIL1 resulted in a significant increase in G:C → T:A transversions caused by the 8-oxo-Gua:C pair in the shuttle plasmid. The knock-down of MUTYH resulted in a reduction in A:T → C:G transversions induced by 8-oxo-dGTP and the 8-oxo-Gua:A pair, but the knockdown of OGG1, NTH1, and NEIL1 had no effect on mutagenesis. These results indicate that all of the above DNA glycosylases suppress mutations caused by 8-oxo-Gua:C in DNA. In contrast, it appears that MUTYH enhances A:T → C:G mutations caused by 8-oxo-dGTP.

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“…Damage to DNA, usually measured as strand breakage, has been shown to occur in many cell types in response to oxidative stress [1][2][3][4][5]. However, little is known about the mechanism of this damage.…”

Section: Introductionmentioning

confidence: 99%

“…However, little is known about the mechanism of this damage. Possible mechanisms include rises in intracellular free Ca 2+ that are sufficient to activate endonucleases [6] and direct attack on DNA by highly reactive radicals, such as hydroxyl, OH ° [2,7,8]. Consistent with direct free radical attack on DNA, several groups have reported increases in 8-hydroxy-2'-deoxyguanosine (8OHdG) in mammalian cells exposed to oxidative stress [1,5,[9][10][11].…”

Section: Introductionmentioning

confidence: 99%

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DNA strand breakage and base modification induced by hydrogen peroxide treatment of human respiratory tract epithelial cells

et al. 1995

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Treatment of human respiratory tract epithelial cellswith H202 led to concentration-dependent DNA strand breakage that was highly-correlated with multiple chemical modifications of all four DNA bases, suggesting that damage is due to hydroxyl radical, OH'. However, the ma|or base damage occurred to adenine. Hence, conclusions made about the occurrence and the extent of oxidative DNA damage on the basis only of changes in 8-hydroxyguanine should be approached with caution.

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DNA damage by oxygen‐derived species Its mechanism and measurement in mammalian systems

Cited by 1,405 publications

References 184 publications

Role of reactive oxygen species in the pathophysiology of human reproduction

Role of reactive oxygen species in the pathophysiology of human reproduction

Effects of base excision repair proteins on mutagenesis by 8-oxo-7,8-dihydroguanine (8-hydroxyguanine) paired with cytosine and adenine

DNA strand breakage and base modification induced by hydrogen peroxide treatment of human respiratory tract epithelial cells

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