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Effects of strontium fructose 1,6‐diphosphate on expression of apoptosis‐related genes and oxidative stress in testes of diabetic rats
Author(s) -
Tang XiaoYun,
Zhang Qi,
Dai DeZai,
Ying HanJie,
Wang QiuJuan,
Dai Yin
Publication year - 2008
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/j.1442-2042.2007.01980.x
Subject(s) - oxidative stress , diabetes mellitus , malondialdehyde , medicine , endocrinology , apoptosis , antioxidant , fructose , streptozotocin , dna fragmentation , glutathione peroxidase , reactive oxygen species , in vivo , andrology , chemistry , biology , superoxide dismutase , biochemistry , programmed cell death , microbiology and biotechnology
Objective: To investigate the effects of strontium fructose 1,6‐diphosphate (FDP‐Sr) on testicular dysfunction induced by diabetes. Methods: Diabetes was induced by a single injection of streptozotocin (65 mg/kg, i.p.). After 28 days, therapy with three doses (50, 100, and 200 mg/kg per day, p.o.) of FDP‐Sr was carried out for another 4 weeks. Results: The rats exhibited morphological lesions of testes and significant decreases in serum testosterone levels after 2 months of diabetes. Testicular tissues of diabetic rats showed significantly increased malondialdehyde levels and declined glutathione peroxidase activity. Meanwhile, augmented DNA fragmentation was observed, along with downregulated Bcl‐2 and upregulated Bax expressions at both mRNA and protein levels. FDP‐Sr showed significant antioxidant effects in both in vitro and in vivo experiments, and significantly relieved apoptosis and the decline of serum testosterone caused by diabetes. Conclusions: Testicular injury and apoptosis induced by diabetes are partially attributed to the augmented oxidative stress in testicular tissue. FDP‐Sr indirectly alleviates these pathologic alterations by suppressing the generation of reactive oxygen species.