Oxidative damage of DNA induced by X-irradiation decreases the uterine endometrial receptivity which involves mitochondrial and lysosomal dysfunction.

نویسندگان

  • Wei Gao
  • Jin-Xiao Liang
  • Shuai Liu
  • Chang Liu
  • Xiao-Fang Liu
  • Xiao-Qi Wang
  • Qiu Yan
چکیده

X irradiation may lead to female infertility and the mechanism is still not clear. After X irradiation exposure, significantly morphological changes and functional decline in endometrial epithelial cells were observed. The mitochondrial and lysosomal dysfunction and oxidative DNA damage were noticed after X irradiation. In addition, pretreatment with NAC, NH4Cl or Pep A reduced the X irradiation induced damages. These studies demonstrate that the oxidative DNA damage which involved dysfunctional lysosomal and mitochondrial contribute to X irradiation-induced impaired receptive state of uterine endometrium and proper protective reagents can be helpful in improving endometrial function.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Involvement of Four Different Intracellular Sites in Chloroacetaldehyde- Induced Oxidative Stress Cytotoxicity

Chloroacetaldehyde (CAA) is a chlorination by-product in finished drinking water and a toxic metabolite of a wide variety of industrial chemicals (e.g. vinyl chloride) and chemotherapeutic agents (e.g. cyclophosphamide and ifosfamide). In this research, the cytotoxic mechanisms of CAA in freshly isolated rat hepatocytes were investigated.CAA cytotoxicity was associated with reactive oxygen spec...

متن کامل

Involvement of Four Different Intracellular Sites in Chloroacetaldehyde- Induced Oxidative Stress Cytotoxicity

Chloroacetaldehyde (CAA) is a chlorination by-product in finished drinking water and a toxic metabolite of a wide variety of industrial chemicals (e.g. vinyl chloride) and chemotherapeutic agents (e.g. cyclophosphamide and ifosfamide). In this research, the cytotoxic mechanisms of CAA in freshly isolated rat hepatocytes were investigated.CAA cytotoxicity was associated with reactive oxygen spec...

متن کامل

Lysosomal Oxidative Stress Cytotoxicity Induced By Para-phenylenediamine Redox Cycling In Hepatocytes

It has already been reported that muscle necrosis induced by various phenylenediamine derivatives are correlated with their autoxidation rate. Now in a more detailed investigation of the cytotoxic mechanism using a model system of isolated hepatocytes and ring-methylated structural isomer durenediamine (DD) we have shown that under aerobic conditions, phenylenediamine induced cytotoxicity and R...

متن کامل

Lysosomal Oxidative Stress Cytotoxicity Induced By Para-phenylenediamine Redox Cycling In Hepatocytes

It has already been reported that muscle necrosis induced by various phenylenediamine derivatives are correlated with their autoxidation rate. Now in a more detailed investigation of the cytotoxic mechanism using a model system of isolated hepatocytes and ring-methylated structural isomer durenediamine (DD) we have shown that under aerobic conditions, phenylenediamine induced cytotoxicity and R...

متن کامل

Curcumin Ameliorates Sodium Valproate Induced Neurotoxicity through Suppressing Oxidative Stress and Preventing Mitochondrial Impairments

Background and purpose: Curcumin is a natural polyphenolic compound in turmeric (Curcuma longa). Curcumin has potent free radical scavenger and antioxidant properties that could significantly reduce oxidative damage. Oxidative stress and mitochondrial dysfunction contribute to valproate sodium induced tissue damage. This study investigated the protective effects of curcumin against valproate so...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • International journal of clinical and experimental medicine

دوره 8 3  شماره 

صفحات  -

تاریخ انتشار 2015