Uncoupling protein 2 combats oxidative damage to human sperm.
- Author:
Zhi-Hong FU
1
;
Yong-Hong ZHOU
;
Wen-Jie ZHU
;
Xiu-Min CHEN
;
Xue-Mei LI
;
Zhen TAN
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Humans; Ion Channels; metabolism; Male; Middle Aged; Mitochondrial Proteins; metabolism; Oxidative Stress; Reactive Oxygen Species; metabolism; Sperm Count; Sperm Motility; Spermatozoa; metabolism; Uncoupling Protein 2
- From: National Journal of Andrology 2010;16(6):516-519
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEGerm cells are much more susceptible to oxidative stress than somatic cells. Accumulating evidence indicates that uncoupling protein 2 (UCP2) prevents the apoptosis of multiple types of cells induced by reactive oxygen species (ROS). The present study aimed to evaluate the protective effect of uncoupling protein 2 (UCP2) against oxidative damage to human sperm.
METHODSSemen parameters were obtained from 97 semen samples by computer assisted sperm analysis (CASA), and the samples, based on the percentage of grade a + b sperm, allotted to Groups I (n = 25, grade a + b sperm > 50%), II (n = 24, grade a + b sperm 25%-50%), III (n = 24, grade a + b sperm 10-25%) and IV (n = 24, grade a + b sperm < 10%). The expressions of sperm UCP2 mRNA was detected by RT-PCR, and the malonaldehyde (MDA) content in ROS was determined in the sperm suspension.
RESULTSThe expressions of UCP2 mRNA in sperm were 1.51 +/- 0.24, 1.28 +/- 0.15, 1.17 +/- 0.20 and 0.69 +/- 0.18, and the MDA contents were (14.66 +/- 2.55), (16.00 +/- 2.09), (17.44 +/- 1.40) and (21.20 +/- 3.50) nmol/10(8) sperm in Groups I, II, III and lV, respectively. There was a significant negative correlation between the expression of UCP2 mRNA and the content of MDA (r = -0.633, P < 0.01), the former obviously reduced while the latter remarkably increased in the groups of lower sperm motility (P < 0.01).
CONCLUSIONUCP2 plays an important protective role against oxidative stress damage to human sperm by diminishing ROS production.