Impact négatif du tabac sur la fertilité masculine : des spermatozoïdes à la descendance

Sepaniak, Sandrine; Forges, Thierry; Fontaine, Bernard; Gérard, Hubert; Foliguet, B; Guillet-May, F.; Zaccabri, A.; Monnier‐Barbarino, Patricia

doi:10.1016/s0368-2315(04)96545-3

Cited by 29 publications

(5 citation statements)

References 27 publications

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“…In addition, OS has been shown to affect the integrity of the sperm chromatin and to cause high frequencies of single and double DNA strand breaks [25]. Previous studies have been indicated that increased sperm nuclear DNA damage strongly and negatively affects natural fertility [26,27]. Furthermore, it has been reported that sperm chromatin/DNA is an independent measure of sperm quality that may have better diagnostic and prognostic capabilities than standard sperm parameters [concentration, motility, and morphology] [28].…”

Section: Oxidative Stress and Reactive Oxygen Speciesmentioning

confidence: 99%

Mechanisms of Male Infertility: Role of Antioxidants

Sheweita

Tilmisany²,

Al-Sawaf

2005

CDM

189

157

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Defective sperm function is the most common cause of infertility, and until recently, was difficult to evaluate and treat. Mammalian spermatozoa membranes are rich in poly unsaturated fatty acids and are sensitive to oxygen induced damage mediated by lipid peroxidation. Hence, free radicals and reactive oxygen species [ROS] are associated with oxidative stress and are likely to play a number of significant and diverse roles in reproduction. The excessive generation of reactive oxygen species by abnormal spermatozoa and by contaminating leukocytes [leukocytospermia] has been identified as one of the few defined etiologies for male infertility. Moreover, environmental factors, such as pesticides, exogenous estrogens, and heavy metals may negatively impact spermatogenesis since male sperm counts were declined. In addition, aging is also likely to further induce oxidative stress. Limited endogenous mechanisms exist to reverse these damages. In a normal situation, the seminal plasma contains antioxidant mechanisms which are likely to quench these ROS and protect against any likely damage to spermatozoa. However, during genitourinary infection/inflammation these antioxidant mechanisms may downplay and create a situation called oxidative stress. Assessment of such oxidative stress status [OSS] may help in the medical treatment of male infertility by suitable antioxidants. The cellular damage in the semen is a result of an improper balance between ROS generation and scavenging activities. Therefore, numerous antioxidants such as vitamin C, vitamin E, glutathione, and coenzyme Q10, have proven beneficial effects in treating male infertility. A multi-faceted therapeutic approach to improve male fertility involves identifying harmful environmental and occupational risk factors, while correcting underlying nutritional imbalances to encourage optimal sperm production and function.

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Section: Oxidative Stress and Reactive Oxygen Speciesmentioning

confidence: 99%

Mechanisms of Male Infertility: Role of Antioxidants

Sheweita

Tilmisany²,

Al-Sawaf

2005

CDM

189

157

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“…In turn, activated Chk phosphorylates a number of downstream effectors to trigger pleiotropic cellular responses, including transcription regulation, alteration of energy consumption, cell-cycle arrest or delay, and DNA repair or cell death if the damage is too severe for repair ( 14 ). The harmful substances in tobacco inhaled by smokers cause DNA damage, which may elevate DNA fragmentation rates ( 15 , 16 ). Increased sperm DNA fragmentation rates have been positively correlated with impaired fertility ( 17 ).…”

Section: Introductionmentioning

confidence: 99%

Potential effect of smoking on semen quality through DNA damage and the downregulation of Chk1 in sperm

Cui¹,

Xuan

Wu³

et al. 2016

Molecular Medicine Reports

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Previous studies have found that smoking is associated with decreased male fertility via altering the quality of semen. However, the mechanism by which cigarette smoking affects semen quality remains to be fully elucidated. Heavy smoking-induced DNA damage has been reported to correlate with abnormal spermatozoa and male infertility. It has been reported that, in response to DNA damage, activation of the checkpoint kinase 1 (Chk1) facilitates S and G2 checkpoint arrest. The aim of the present study was to investigate the expression levels of Chk1 in sperm cells of smoking and non-smoking men, and to further examine the correlation between DNA fragmentation rates and the expression levels of Chk1 with smoking. The present study was performed on a cohort of 841 smoking men and 287 non-smoking men. In the investigation, sperm concentration, motility, viability, seminal plasma zinc concentration, acrosin activity and sperm DNA fragmentation were examined. The gene and protein expression levels of Chk1 were detected using reverse transcription quantitative-polymerase chain reaction and western blot analyses, respectively. It was observed that the progressive motility of the sperm was significantly decreased in the moderate and heavy smoking groups, whereas no significant changes were observed in the mild smoking group. The sperm in the medium-term smoking group had significantly decreased progressive motility, and the semen concentration, sperm count and progressive motility vitality were markedly decreased in the long-term smoking group. Compared with the non-smoking group, the abnormal head rates in the heavy smoking group and long-term smoking group were significantly increased. The sperm viability and seminal plasma zinc concentration were markedly increased in the smoking group. Increased DNA fragmentation rates were found in the smoking group. The expression of Chk1 was significantly decreased in the smoking group, compared with the non-smoking group. Progressive motility and sperm concentration showed a nonlinear association with the relative mRNA expression of Chk1. However, an inverse association was found between DNA fragmentation rates and the progressive motility and sperm concentration. These data suggested that the decrease of semen quality caused by cigarette smoking was not only correlated with sperm DNA fragmentation rates, but was also correlated with a decline in the expressive level of Chk1. The expression of Chk1 was associated with DNA damage and apoptosis, the reduction of which may lead to decreased sperm repair and increased sperm apoptosis, with a subsequent effect on semen quality.

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“…The presence of these components in the seminal plasma may induce a degradation of sperm parameters and nuclear quality of spermatozoa, and compromise the chances of pregnancy. [15].…”

Section: Discussionmentioning

confidence: 99%