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Progressively motile human spermatozoa are well protected against in vitro lipid peroxidation imposed by induced oxidative stress
Author(s) -
Rhemrev J. P. T.,
Vermeiden J. P. W.,
Haenen G. R. M. M.,
De Bruijne J. J.,
RekersMombarg L. T. M.,
Bast A.
Publication year - 2001
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1046/j.1439-0272.2001.00430.x
Subject(s) - lipid peroxidation , oxidative stress , thiobarbituric acid , andrology , semen , population , chemistry , reactive oxygen species , motility , tbars , biochemistry , biology , microbiology and biotechnology , medicine , environmental health
Summary. Semen samples of 24 patients were analysed. Volumes were measured and the numbers of progressively motile (PMS), motile (MS) and nonmotile spermatozoa (NMS) were determined. These 24 samples appeared to show a large variation in motility percentages and numbers. Spermatozoa of these semen samples were isolated from the seminal plasma and exposed to induced radical oxygen stress imposed by iron/ascorbate. Lipid peroxidation (LPO) was quantified as thiobarbituric acid reactive material. The contributions of PMS, MS and NMS were also estimated. It was found that the PMS did not contribute to the formation of lipid peroxides. The cellular radical defence system of PMS may offer them adequate protection against the harsh conditions of radical oxygen stress. Stepwise regression analyses showed that only the population of NMS contributed significantly to the explanation of the variance in LPO production ( R 2 = 0.56, P < 0.001). Pre‐existing membrane lipid peroxides were not detected in spermatozoa. It is therefore suggested that LPO takes place only after radical oxygen stress has exhausted the cellular defence system. LPO is not the initial, but one of the later, events leading to the death of spermatozoa. It is concluded that the population of progressively motile spermatozoa in semen samples does not contribute to the production of thiobarbituric acid reactive substances as induced by in vitro radical oxygen stress.