Superoxide dismutase content and fatty acid composition in subsets of human spermatozoa from normozoospermic, asthenozoospermic, and polyzoospermic semen samples

Human ejaculated sperm comprised discrete subsets of spermatozoa, with different degrees of maturation. These subpopulations can be isolated through density gradient centrifugation. Sperm from the lowest density layer show the highest content of docosahexaenoic acid and sterols, and produce the highest levels of reactive oxygen species. The main objective of this study was to determine the superoxide dismutase (SOD) content and fatty acid composition of subsets of spermatozoa isolated from normozoospermic, asthenozoospermic, and polyzoospermic semen samples. Four sperm fractions (1-4) were obtained using ISolate gradient centrifugation. Morphology, motion parameters, SOD content, and fatty acid composition were assessed in the original samples and their fractions. Overall, sperm from normozoospermic samples had higher SOD content than those of asthenozoospermic or polyzoospermic samples. Once fractionated in subsets, the sperm SOD content decreased significantly (P < 0.0001) from fraction 1 (top) to 4 (bottom) in all three groups of samples. Fatty acid content as well as the oxidation coefficient followed the same pattern, decreasing from fraction 1 to 4 (F1-F4). Normo- and polyzoospermic samples showed similar amounts of fatty acids, while asthenozoospermic samples mostly revealed increased levels. Normozoospermic samples displayed the lowest unsaturated fatty acid (UFA)/SOD ratio. Spermatozoa from astheno- and polyzoospermic samples, two common seminal pathologies, showed higher UFA and lower SOD content than normal sperm, therefore exhibiting a higher susceptibility to peroxidative damage. F4 from all groups, containing the most mature spermatozoa, displayed the lowest polyunsaturated fatty acid and SOD content of all subsets, suggesting that excessive SOD activity as well as abundant peroxidative targets may both be deleterious to sperm function. (C) 2003 Wiley-Liss, Inc.