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Sperm Function Test

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Toxicity arising from excess exposure to oxygen (O2) is an inherent challenge to aerobic life. The harmful effects of O2 are attributed to its reduced form (superoxide radical: O2-) or its by-products combined with other highly unstable molecules (hydrogen peroxide: H2O2; hydroxyl radical: HO-). These substances, called oxygen free radicals (from English Reactive Oxygen Species; ROS) have harmful effects in cascade with the surrounding cells in an almost instantaneous way. Cell survival in the face of free radical attack depends, therefore, on the balance between the processes of production and elimination of ROS.


Any circumstance that unbalances these two processes can induce the installation of a condition called oxidative stress, in which the formation of free radicals (oxidizing agents) to antioxidants prevails.



The acrosome is the region of the head of the sperm that is membrane-coated and composed of enzymes. These enzymes have the biological function of breaking down the cell layers that surround the oocyte (Cumulus oophorus and zona pellucida), thus allowing sperm penetration and fertilization. The release of these enzymes is called an acrosome reaction.

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Sperm without mitochondrial activity.


The sperm membrane is composed of polyunsaturated and target fatty acids (PUFAs) that guarantee the necessary fluidity for its movement during the fertilization process. Due to their chemical composition, PUFAs are targets of oxygen free radicals (ROS), small molecules from sperm metabolism and from external sources such as leukocytes present in genitourinary tract infections, drug abuse, or varicocele. Under normal conditions, ROS are countered by a defense system made up of antioxidants, however, several medical conditions can reduce the antioxidant capacity or increase the production of ROS. When the antioxidant capacity is ineffective, ROS initiate an attack on the sperm membrane and initiate a cascade of cellular changes that compromise their fertilization potential. Therefore, membrane changes are early markers of sperm changes.

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  • Hrudka F. Cytochemical and ultracytochemical demonstration of cytochrome c oxidase in spermatozoa and dynamics of its changes accompanying aging or induced by stress. Int J Androl, v.10, p.809-828, 1987.

  • Franceschi C. Mitochondrial membrane potential and DNA stainability in human sperm cells: a flow cytometry analysis with implications for male infertility. Exp Cell Res, v.241, p.384-393, 1998.

  • Bourgeron T: Mitochondrial function and male infertility. Results and Problems in Cell Differentiation 28: 187–210, 2000.

  • Koppers AJ, De Iuliis GN, Finnie JM, Mclaughlin E A, Aitken RJ. Significance of mitochondrial reactive oxygen species in the generation of oxidative stress in spermatozoa. J Clin Endocrinol Metab, v.93, p.3199-3207, 2008.

  • Hu Y, Xia X, Pan L, Lu N, Wu Y, Zhou X, Shang X, Cui Y, Huang Y. Evaluation of sperm mitochondrial membrane potential in varicocele patients using JC-1 fluorescent staining. Nat J Androl, v.15, p.792-795, 2009.

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