Candelario-Jalil E, Mohammed-Al-Dalain S, Fernández O S, Menéndez S, Pérez-Davison G, Merino N, Sam S, Ajamieh H H
Center for Research and Biological Evaluation, University of Havana, Institute of Pharmacy and Food Sciences, Apartado Postal 6079, Havana City 10600, Cuba.
J Appl Toxicol. 2001 Jul-Aug;21(4):297-301. doi: 10.1002/jat.758.
The rectal insufflation of a judicious dose of ozone, selected from that used in clinical practice, is able to promote oxidative preconditioning or oxidative stress tolerance preventing the hepatocellular damage mediated by free radicals. In order to evaluate the effects of ozone oxidative preconditioning on carbon tetrachloride-mediated hepatotoxicity, the following experimental protocol was designed: group 1 (negative control, sunflower oil i.p.); group 2 (CCl(4) in sunflower oil, 1 ml kg(-1) i.p.); group 3 (15 ozone-oxygen pretreatments at a dose of 1 mg kg(-1) via rectal insufflation + CCl(4) as in group 2); group 4 (ozone control group, 15 ozone-oxygen pretreatments + sunflower oil i.p.). Ozone pretreatment prevented glycogen depletion (as demonstrated by biochemical and histopathological findings) and avoided lactate overproduction associated with the hepatotoxic effects of CCl(4). The administration of CCl(4) increased lipid peroxidation (as measured by thiobarbituric acid-reactive substances) and uric acid levels and inhibited superoxide dismutase activity. All these deleterious effects induced by CCl(4) were prevented by ozone pretreatment. The administration of ozone without CCl(4) (ozone control group) did not produce any changes in the evaluated parameters. Our results showed that ozone treatment, in our experimental conditions, was able to prevent anaerobic glycolysis and oxidative stress induced by CCl(4).
从临床实践中选用合适剂量的臭氧进行直肠注入,能够促进氧化预处理或氧化应激耐受,预防自由基介导的肝细胞损伤。为了评估臭氧氧化预处理对四氯化碳介导的肝毒性的影响,设计了以下实验方案:第1组(阴性对照组,腹腔注射葵花籽油);第2组(腹腔注射1 ml·kg⁻¹ 溶于葵花籽油的四氯化碳);第3组(通过直肠注入1 mg·kg⁻¹ 的剂量进行15次臭氧 - 氧气预处理 + 如第2组的四氯化碳);第4组(臭氧对照组,15次臭氧 - 氧气预处理 + 腹腔注射葵花籽油)。臭氧预处理可防止糖原耗竭(生化和组织病理学结果证明),并避免与四氯化碳肝毒性相关的乳酸过度产生。四氯化碳的给药增加了脂质过氧化(通过硫代巴比妥酸反应性物质测量)和尿酸水平,并抑制了超氧化物歧化酶活性。臭氧预处理可预防四氯化碳诱导的所有这些有害影响。在无四氯化碳的情况下给予臭氧(臭氧对照组)未使评估参数发生任何变化。我们的结果表明,在我们的实验条件下,臭氧处理能够预防四氯化碳诱导的无氧糖酵解和氧化应激。