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Sperm Function Test

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OXYGEN FREE RADICALS

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.

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ACROMOSOMIC REACTION

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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LIPID PEROXIDATION

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.

References:

  • Ohkawa H, Ohishi N, Yagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem. 1979 Jun;95(2):351-8. 

  • Alvarez JG, Storey BT. Assessment of cell damage caused by spontaneous lipid peroxidation in rabbit spermatozoa. Biol Reprod. 1984 Mar;30(2):323-31.

  • Valenzuela A. The biological significance of malondialdehyde determination in the assessment of tissue oxidative stress. Life Sci. 1991;48(4):301-9.

  • Huszar G, and Vigue L: Correlation between the rate of lipid peroxidation and cellular maturity as measured by creatine kinase activity in human spermatozoa. J Androl 15: 71–77, 1994.

  • Laudat A, Lecourbe K, Guechot J, Palluel AM. Values of sperm thiobarbituric acid-reactive substance in fertile men. Clin Chim Acta. 2002 Nov;325(1-2):113-5.

  • Hallak, J., Pariz, JR The Role of the Andrologist in an Intrauterine Insemination Program in Intrauterine Insemination (pp,483-500), 2013. Edition: 3rd edition Publisher: Jaypee Brothers Medical Pub - ISBN: 978-9350904039

  • Silva EJR, Ribeiro CM, Mirim AFM, Silva AAS, Romano RM, Hallak J, Avellar MCW. Lipopolysaccharide and lipotheic acid differentially modulate epididymal cytokine and chemokine profiles and sperm parameters in experimental acute epididymitis. Sci Rep. 2018 Jan 8;8(1):103. 

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