Smoking and low antioxidant levels increase oxidative damage to sperm DNA

Fraga, César G.; Motchnik, Paul A.; Wyrobek, Andrew J.; Rempel, David; Ames, Bruce N.

doi:10.1016/0027-5107(95)00251-0

Cited by 421 publications

(212 citation statements)

References 15 publications

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“…This study provides considerable support, therefore, to the hypothesis that parental cigarette smoking is a risk factor for childhood hepatoblastoma . It is possible to speculate that the importance of both parents smoking in the aetiology of hepatoblastoma might arise from the combination of oxidative damage to sperm DNA (Fraga et al, 1996) and damage to the fetal liver from carcinogenic metabolites in the blood of the pregnant mother. Obtained from unconditional logistic regression using all controls as comparison group.…”

Section: Discussionmentioning

confidence: 99%

Parental cigarette smoking and childhood risks of hepatoblastoma: OSCC data

Sorahan

Lancashire

2004

Br J Cancer

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Reported cigarette smoking habits for the parents of 43 UK children who died with hepatoblastoma (1953 -55 deaths, 1971 -81 deaths) have been compared with corresponding information for the parents of 5777 healthy control children by means of unconditional logistic regression. Hepatoblastoma risks were doubled if both parents smoked relative to neither parent smoking (RR 2.28, 95% CI 1.02 -5.09).

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Section: Discussionmentioning

confidence: 99%

Parental cigarette smoking and childhood risks of hepatoblastoma: OSCC data

Sorahan

Lancashire

2004

Br J Cancer

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“…Oxidative stress has also been correlated with high frequencies of single and double DNA strand breaks (72,74). Strong evidence suggests that high levels of ROS mediate the DNA fragmentation commonly observed in spermatozoa of infertile men (75)(76)(77)(78). This information has important clinical implications, particularly in the context of ARTs.…”

Section: Oxidative Stress-induced Dna Damagementioning

confidence: 98%

Role of reactive oxygen species in the pathophysiology of human reproduction

Agarwal

Saleh

Bedaiwy

2003

Fertility and Sterility

1,286

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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“…Due to its mutagenic potential, 8OHdG has been widely suggested as a biomarker for various cancers [12][13][14]. The concentration of 8OHdG is also evaluated in smokers and non-smokers [9,15,16] since cigarette smoke contains a large amount of oxygen radical forming substances, such as catechol and hydroquinone that may enhance lung carcinogenesis by free radical-mediated reactions. Loft et al [9] reported smokers excreted 50% more 8OHdG than non-smokers in 24 h urine, indicating a 50% increased rate of oxidative DNA damage from smoking.…”

Section: Introductionmentioning

confidence: 99%