Oxidative stress and free radical damage in patients with acute dipterex poisoning.

نویسندگان

  • Jun-Fu Zhou
  • Wen Zhou
  • Shu-Mei Zhang
  • Yan-Er Luo
  • Huai-Hong Chen
چکیده

OBJECTIVE To investigate whether acute dipterex poisoning (ADP) may cause oxidative stress and free radical damage in the bodies of acute dipterex poisoning patients (ADPPs), and to explore the mechanisms by which ADP may cause oxidative stress and free radical damage. METHODS Fifty ADPPs and fifty healthy adult volunteers (HAVs) whose ages, gender and others were matched with the ADPPs were enrolled in a randomized controlled study, in which concentrations of nitric oxide (NO), vitamin C (VC), vitamin E (VE) and beta-carotene (beta-CAR) in plasma as well as concentration of lipoperoxide (LPO), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric analytical methods. RESULTS Compared with the average values of experimental parameters in the HAVs group, the average values of plasma NO and erythrocyte LPO in the ADPPs group were significantly increased (P<0.0001), while those of plasma VC, VE and beta-CAR as well as erythrocyte SOD, CAT, GPX and AChE in the ADPPs group were significantly decreased (P<0.0001). Bivariate correlation analysis and partial correlation analysis suggested that when NO and LPO values were increased, and VC, VE, beta-CAR, SOD, CAT and GPX values were decreased in the ADPPs, AChE value was decreased gradually in the ADPPs (P<0.001-0.0001). Reliability analysis of experimental parameters reflecting oxidative stress and free radical damage in the ADPPs showed that the reliability coefficient (8 items) alpha=0.6909, and the standardized item alpha=0.8574. CONCLUSION The findings in the present study suggest that ADP can cause oxidative stress and free radical damage, and inhibit markedly erythrocyte acetylcholinesterase activity in ADPPs.

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عنوان ژورنال:
  • Biomedical and environmental sciences : BES

دوره 17 2  شماره 

صفحات  -

تاریخ انتشار 2004