title: Cigarette smoking affects specific sperm oxidative defenses but does not cause oxidative DNA damage in infertile men.
abstract: OBJECTIVE
  To evaluate the effects of tobacco consumption on the oxidative defenses of sperm, the glutathione system (GS), and sperm DNA oxidation.
  
  
  METHODS
  Double-blind experimental study.
  
  
  METHODS
  Andrology laboratory in a university-affiliated private setting.
  
  
  METHODS
  One hundred seventeen semen samples from infertile males.
  
  
  METHODS
  None.
  
  
  METHODS
  (a) sperm GS enzymatic activity with respect to glutathione peroxidase isoforms GPx-1 and GPx-4, glutathione reductase (GR), and cellular glutathione (GSH) content (n = 29); (b) GPx-1, GPx-4, and GR mRNA expression analysis (n = 33); (c) oxidative DNA damage quantification using OXIDNA assay kit (n = 55). Two groups were established: nonsmoking and smoking males. The t tests were employed to detect significant differences between groups.
  
  
  RESULTS
  We identified a significant decrease in sperm GPx-4 activity but not in GPx-1 and GSH activity in smokers compared with nonsmokers. A significant decrease was also observed in GPx-1, GPx-4, and GR mRNA expression in the former group. Interestingly, we did not observe any significant variation in the percentage of cells with oxidative damage of the DNA or in the average level of oxidation of affected cells with respect to the smoking condition of the male.
  
  
  CONCLUSIONS
  We demonstrate that smoking has a negative impact on intracellular antioxidant enzymes but that effect does not increase oxidative DNA damage. Thus, the effects of reduced oxidative defenses in sperm as a result of cigarette smoking are yet to be elucidated.
authors.affiliation: IVI Valencia, Universidad de Valencia, Valencia, Spain. tviloria@ivi.es
authors.forename: Thamara
authors.initials: T
authors.lastname: Viloria
authors.forename: Marcos
authors.initials: M
authors.lastname: Meseguer
authors.forename: José Antonio
authors.initials: JA
authors.lastname: Martínez-Conejero
authors.forename: J E
authors.initials: JE
authors.lastname: O'Connor
authors.forename: José
authors.initials: J
authors.lastname: Remohí
authors.forename: Antonio
authors.initials: A
authors.lastname: Pellicer
authors.forename: Nicolás
authors.initials: N
authors.lastname: Garrido
mesh_terms: D004249:DNA Damage / Q000502:physiology*; D015971:Gene Expression Regulation, Enzymologic; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D005980:Glutathione Reductase / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007248:Infertility, Male / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D012333:RNA, Messenger / Q000378:metabolism; D012907:Smoking / Q000009:adverse effects*; D013094:Spermatozoa / Q000378:metabolism* / Q000473:pathology; D000094765:Glutathione Peroxidase GPX1
chemical_list: D012333:RNA, Messenger; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005978:Glutathione; D000094765:Glutathione Peroxidase GPX1; C000722067:GPX1 protein, human