<p>The efficiency of ascorbic acid (ASCB) as an antioxidant protective drug is affected by the treatment model utilized. Our previous studies showed that ASCB co-treatment does not protect the testis of rats in a busulfan model of testicular injury. This study compared the effect of ASCB in a pretreatment, post-treatment, and co-treatment models of busulfan-induced testicular injury. Forty Wistar rats were randomly assigned into five groups of 8 animals per each group: control, busulfan (10&#xa0;mg&#xa0;kg<sup>−1</sup> body weight (bw) injected intraperitoneally on day 14); ASCB pre-treatment (100&#xa0;mg&#xa0;kg<sup>−1</sup> bw for 14&#xa0;days before busulfan injection begins on day 14, and then ASCB oral gavage continued until end of study); ASCB co-treatment (100&#xa0;mg&#xa0;kg<sup>−1</sup> bw of ASCB administered concurrently with busulfan, 10&#xa0;mg&#xa0;kg<sup>−1</sup> bw); and post-treatment (100&#xa0;mg&#xa0;kg<sup>−1</sup> bw of ASCB was administered 14&#xa0;days after busulfan injection, 10&#xa0;mg&#xa0;kg<sup>−1</sup> bw) on day 1. In all treatment models, ASCB treatment continues for 39&#xa0;days when the study was terminated. At the end of the study, ASCB pre-treatment increased glutathione concentration; improved sperm motility, count, and morphology; and decreased catalase activity, lipid peroxidation, and DNA fragmentation relative to the busulfan values (<i>P</i> &lt; 0.05). ASCB co-treatment reduced superoxide dismutase activity, decreased H<sub>2</sub>O<sub>2</sub> generation, and increased catalase activity and nitrite concentration much more than busulfan values, whereas ASCB post-treatment decreased gonadosomatic index, absolute testis weight, and testicular glutathione concentration, and increased DNA damage. ASCB pretreatment decreased whereas its co-treatment and post-treatment exacerbated busulfan-induced testicular oxidative damage and spermatological toxicity.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Protective effects of ascorbic acid on busulfan-induced oxidative damage and testicular function in Wistar rats

  • Justina C. Nwokoma,
  • Chioma J. Okonkwo,
  • Eka B. Essien,
  • Ogechukwu E. Ezim,
  • Chisom E. Nebeolisa,
  • Chinedu J. Okonkwo,
  • Joy Nyeche,
  • Victoria C. Obinna,
  • Sunny O. Abarikwu

摘要

The efficiency of ascorbic acid (ASCB) as an antioxidant protective drug is affected by the treatment model utilized. Our previous studies showed that ASCB co-treatment does not protect the testis of rats in a busulfan model of testicular injury. This study compared the effect of ASCB in a pretreatment, post-treatment, and co-treatment models of busulfan-induced testicular injury. Forty Wistar rats were randomly assigned into five groups of 8 animals per each group: control, busulfan (10 mg kg−1 body weight (bw) injected intraperitoneally on day 14); ASCB pre-treatment (100 mg kg−1 bw for 14 days before busulfan injection begins on day 14, and then ASCB oral gavage continued until end of study); ASCB co-treatment (100 mg kg−1 bw of ASCB administered concurrently with busulfan, 10 mg kg−1 bw); and post-treatment (100 mg kg−1 bw of ASCB was administered 14 days after busulfan injection, 10 mg kg−1 bw) on day 1. In all treatment models, ASCB treatment continues for 39 days when the study was terminated. At the end of the study, ASCB pre-treatment increased glutathione concentration; improved sperm motility, count, and morphology; and decreased catalase activity, lipid peroxidation, and DNA fragmentation relative to the busulfan values (P < 0.05). ASCB co-treatment reduced superoxide dismutase activity, decreased H2O2 generation, and increased catalase activity and nitrite concentration much more than busulfan values, whereas ASCB post-treatment decreased gonadosomatic index, absolute testis weight, and testicular glutathione concentration, and increased DNA damage. ASCB pretreatment decreased whereas its co-treatment and post-treatment exacerbated busulfan-induced testicular oxidative damage and spermatological toxicity.