title: Sperm DNA fragmentation and oxidation are independent of malondialdheyde.
abstract: BACKGROUND
  There is clinical evidence to show that sperm DNA damage could be a marker of sperm quality and extensive data exist on the relationship between DNA damage and male fertility status. Detecting such damage in sperm could provide new elements besides semen parameters in diagnosing male infertility. We aimed to assess sperm DNA fragmentation and oxidation and to study the association between these two markers, routine semen parameters and malondialdehyde formation.
  
  
  METHODS
  Semen samples from 55 men attending the Histology-Embryology Laboratory of Sfax Faculty of Medicine, Tunisia, for semen investigations were analysed for sperm DNA fragmentation and oxidation using flow cytometry. The Sperm was also assessed spectrophotometrically for malondialdehyde formation.
  
  
  RESULTS
  Within the studied group, 21 patients were nonasthenozoospermic (sperm motility ≥ 50%) and 34 patients were considered asthenozoospermic (sperm motility < 50%). A positive correlation was found between sperm DNA fragmentation and oxidation (p = 0.01; r = 0.33). We also found a negative correlation between sperm DNA fragmentation and some sperm parameters: total motility (p = 0.001; r = -0.43), rapid progressive motility (type a motility) (p = 0.04; r = -0.27), slow progressive motility (type b motility) (p = 0.03; r = -0.28), and vitality (p < 0.001; r = -0.65). Sperm DNA fragmentation was positively correlated with coiled tail (p = 0.01; r = 0.34). The two parameters that were found to be correlated with oxidative DNA damage were leucocytes concentrations (p = 0.01; r = 0.38) and broken neck (p = 0.02; r = 0.29). Sperm MDA levels were negatively correlated with sperm concentration (p < 0.001; r = -0.57), total motility (p = 0.01; r = -0.35) and type a motility (p = 0.03; r = -0.32); but not correlated with DNA fragmentation and DNA oxidation.
  
  
  CONCLUSIONS
  Our results support the evidence that oxidative stress plays a key role in inducing DNA damage; but nuclear alterations and malondialdehyde don't seem to be synchronous.
authors.affiliation: Laboratory of Human Molecular Genetics, Sfax Faculty of Medicine, Avenue Magida Boulila 3028 Sfax, Tunisia. nacira.zribi@gmail.com
authors.forename: Nassira
authors.initials: N
authors.lastname: Zribi
authors.forename: Nozha Feki
authors.initials: NF
authors.lastname: Chakroun
authors.forename: Henda
authors.initials: H
authors.lastname: Elleuch
authors.forename: Fatma Ben
authors.initials: FB
authors.lastname: Abdallah
authors.forename: Afifa Sellami
authors.initials: AS
authors.lastname: Ben Hamida
authors.forename: Jalel
authors.initials: J
authors.lastname: Gargouri
authors.forename: Faiza
authors.initials: F
authors.lastname: Fakhfakh
authors.forename: Leila Ammar
authors.initials: LA
authors.lastname: Keskes
mesh_terms: D000328:Adult; D053627:Asthenozoospermia / Q000235:genetics; D004249:DNA Damage; D053938:DNA Fragmentation; D006801:Humans; D020287:In Situ Nick-End Labeling; D007248:Infertility, Male / Q000235:genetics*; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism*; D008875:Middle Aged; D010084:Oxidation-Reduction; D055101:Semen Analysis; D013081:Sperm Motility / Q000235:genetics; D013094:Spermatozoa / Q000187:drug effects / Q000378:metabolism*
chemical_list: D008315:Malondialdehyde