Inflammatory mediators exert toxic effects of oxidative stress on human spermatozoa

J Androl. 2007 Mar-Apr;28(2):325-33. doi: 10.2164/jandrol.106.001149. Epub 2006 Nov 1.

Abstract

Epidemiological studies regarding male infertility have revealed that more and more infertile men suffer from acute or chronic inflammation of the genitourinary tract, which often occurs without any symptoms. The inflammatory reactions within the male genital tract are inevitably connected with oxidative stress. Growing evidence indicates that imbalance between prooxidative and anti-oxidative substances in semen leads to metabolic and functional disorders of male germ cells and may be a primary cause of some types of infertility. The infectious factor and local tissue damage can lead to the infiltration of leukocytes to the inflammatory site. This is in an obvious way connected to the production and release of large amounts of reactive oxygen species (ROS), which trigger immune responses directed against the infectious agent, and the simultaneous secretion of numerous biological substances, thereby escalating the inflammation. Some of these factors are proteases and proinflammatory cytokines. Extended exposure of spermatozoa to ROS may lead to the peroxidation of sperm membrane lipids. Many studies point to the combined activities of inflammatory mediators in exerting toxic effects on spermatozoa. The local influences of biologically active substances released by activated leukocytes in the course of the inflammatory response and the mutual interactions of various factors (bacteria, leukocytes, proinflammatory cytokines) at the site represent a complex puzzle.

Publication types

  • Review

MeSH terms

  • Bacterial Infections / physiopathology*
  • Genital Diseases, Male / physiopathology*
  • Genitalia, Male / drug effects*
  • Humans
  • Inflammation Mediators / physiology*
  • Interleukins / physiology
  • Leukocytes / physiology
  • Male
  • Oxidative Stress / physiology*
  • Semen / cytology
  • Spermatozoa / drug effects*
  • Tumor Necrosis Factor-alpha / physiology

Substances

  • Inflammation Mediators
  • Interleukins
  • Tumor Necrosis Factor-alpha