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Oyster peptide prevents the occurrence of exercise‐hypogonadal male condition by improving the function of pituitary gonadal axis in male rats
Author(s) -
Jin Qiguan,
Shi Wenting,
Wang Yuchen,
Li Shuyan,
Xue Chen,
Xu Haoran,
Wu Meitong,
Wei Ying
Publication year - 2021
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.14005
Subject(s) - endocrinology , medicine , sperm , epididymis , sperm motility , biology , andrology , glutathione peroxidase , cholesterol side chain cleavage enzyme , testosterone (patch) , steroidogenic acute regulatory protein , follicle stimulating hormone , superoxide dismutase , hormone , luteinizing hormone , oxidative stress , gene expression , metabolism , cytochrome p450 , biochemistry , gene
This study evaluates the protective role of oyster peptide (OP) on the occurrence of Exercise‐Hypogonadal Male Condition. Male rats were given heavy‐load swimming training and / or OP was supplemented for 6 consecutive weeks. After heavy‐load training, sperm count, sperm viability and sperm motility in epididymis, testosterone in serum and testis, glutathione peroxidase (GSH‐px) and androgen receptor (AR) in testis and mating times were remarkably decreased, malondialdehyde (MDA), capture latency and mating latency were significantly increased, mRNA expression of steroidogenic acute regulatory (StAR) and P450 cholesterol side‐chain cleavage enzyme (P450scc) were obviously down‐regulated, but serum follicle‐stimulating hormone (FSH) and luteinising hormone (LH) were not statistically changed. Conversely, when OP was supplemented at heavy‐load training, sperm count, sperm viability and sperm motility in epididymis, serum FSH, LH, testosterone, GSH‐px, superoxide dismutase (SOD), testosterone, AR in testis and mating times were dramatically increased, while testicular MDA, capture latency and mating latency were significantly decreased, and mRNA expression of StAR, StARD7, P450scc and 3β‐hydroxysteroid dehydrogenase (3β‐HSD) were significantly up‐regulated. In conclusion, heavy‐load training causes testicular spermatogenic and steroidogenic disorders by enhancing the generation of reactive oxygen species (ROS), which can be protected by the co‐administration of OP by enhancing the function of pituitary gonad axis and lowering ROS generation.