Effects of Aerobic Exercise Combined with Oyster Peptide Supplement on the Formation of CTX-induced Late-Onset Hypogonadism in Male Rats.
Wenting ShiYu LiuQi-Guan JinMeitong WuQizheng SunZheng LiWenying LiuPublished in: Reproductive sciences (Thousand Oaks, Calif.) (2022)
The purpose of this study is to investigate the effect of aerobic exercise (AE) training and/or oyster peptide (OP) supplementation on the formation of late-onset hypogonadism (LOH). AE training and/or OP supplement was performed during Cytoxan (CTX)-induced LOH formation in male SD rats for 6 consecutive weeks. Low dose of CTX could decrease mating times, the levels of luteinizing hormone (LH), total testosterone (TT), free testosterone (FT) in serum and TT, androgen receptor (AR), androgen binding protein (ABP), and glutathione peroxidase (GSH-Px) in testicle, but increase capture latency, mating latency, and malondialdehyde, and downregulate the mRNA expression of steroidogenic acute regulatory (StAR), P450 cholesterol side chain cleavage enzyme (P450scc), and StAR-related lipid transfer domain 7 (StARD7) in testicle. Every change was altered by AE training combined with OP supplement significantly, except for serum LH. Moreover, the effect of AE training combined with OP supplement was better than that of AE training on serum TT, FSH, testicular TT, mating latency, capture times, and mating times. AE training combined with OP supplement during CTX-induced LOH formation can prevent the LOH development by enhancing pituitary-gonads axis's function and reducing testicular oxidative stress to promote testosterone synthesis and spermatogenesis.
Keyphrases
- late onset
- virtual reality
- diabetic rats
- oxidative stress
- replacement therapy
- low dose
- early onset
- drug induced
- high glucose
- klebsiella pneumoniae
- binding protein
- high dose
- intensive care unit
- hydrogen peroxide
- transcription factor
- hepatitis b virus
- ischemia reperfusion injury
- multidrug resistant
- smoking cessation
- extracorporeal membrane oxygenation
- germ cell
- endoplasmic reticulum stress