Medical ozone therapy decreases postoperative uterine adhesion formation in rats.

PURPOSE: Various studies have been performed to find out novel treatment strategies to prevent postoperative adhesion formation. Ozone therapy (OT) is shown to reduce inflammation in several pathological conditions. Therefore, we aimed to evaluate the efficacy of OT in a rat model of experimental uterine adhesion (EUA). METHODS: Thirty female Wistar rats (200-250 g) were divided into three groups: sham, EUA and EUA+OT. EUA and EUA+OT groups were subjected to the postoperative adhesion procedure by bipolar coagulation on the uterine horns and corresponding pelvic sidewall parietal peritoneum. EUA+OT group received 0.7 mg/kg daily single dose for 3 days of ozone/oxygen mixture intraperitoneally after adhesion induction. All animals were killed on the 7th day and uterine adhesions were scored. Uterine tissues and peritoneal washing fluid were harvested for all analyses. RESULTS: Uterine malondialdehyde levels in the EUA group were significantly higher compared to the other groups. However, in the EUA group, uterine superoxide dismutase and glutathione peroxidase activities were lower than in other groups. Peritoneal fluid TNF-α levels were found to be significantly different for all groups (p < 0.001). Macroscopic total adhesion score was significantly higher in the EUA group compared to the other groups (p < 0.001). But, total score in the EUA+OT group was lower than in the EUA group (p = 0.006). CONCLUSIONS: Medical OT prevents postoperative uterine adhesions by modulating TNF-α levels and oxidative/antioxidative status in an experimental uterine adhesion model.

Ozone therapy prevents renal inflammation and fibrosis in a rat model of acute pyelonephritis.

INTRODUCTION: Not only bacterial characteristics but also oxidative/nitrosative stress could play a significant role in renal parenchymal inflammatory processes in acute pyelonephritis (APN). This study was conducted to evaluate the effect of ozone therapy (OT), as an immunomodulator and antioxidant, on the renal function, morphology and biochemical parameters of oxidative stress in an experimental model of APN in rats. MATERIALS AND METHODS: Forty rats were divided equally into five groups as control, APN, APN + Antibiotic, APN + OT, and APN + Antibiotic + OT. APN was induced by 0.1 ml of freshly prepared Escherichia coli (ATCC 25922) solution containing 10(10) colony-forming unit/ml into the kidney. A control group was administered 0.1 ml of 0.9 % NaCl solution. Treatment was begun 72 h after bacterial inoculation. Control and APN groups were given 0.9% NaCl solution, APN + Antibiotic and APN + OT were given either antibiotic (ciprofloxacine 150 mg/kg intramuscular/twice daily) or OT. APN + Antibiotic + OT group was given both antibiotic and OT for five consecutive days. At the end of the seventh day, animals were killed via decapitation and trunk blood was collected. Both kidneys were harvested and one half of each kidney were immediately stored for antioxidant enzyme activity, tissue lipid peroxidation and protein carbonyl content. The remainder was fixed for histopathologic examination. RESULTS: E. coli-induced APN increased the renal glomerular and tubular dysfunction, oxidative stress parameters and antioxidant enzyme activities. Either antibiotherapy or OT markedly ameliorated renal dysfunction, the antioxidant status of the kidneys and histopathological injuries subjected to E. coli-induced APN. Interestingly, the combination of antibiotherapy and OT was much more effective than either of the treatment modalities alone. CONCLUSION: The combination of antibiotherapy and OT markedly ameliorated renal dysfunction and improved antioxidant status and histopathologic modalities in rats subjected to E. coli-induced APN than either antibiotherapy or OT treatment alone. Therefore, OT may be considered as an adjuvant therapy to classical antibiotherapy to prevent renal inflammation and fibrosis in APN.

Effects of medical ozone therapy on acetaminophen-induced nephrotoxicity in rats.

Acetaminophen (APAP), also known as paracetamol, is the commonest cause of toxic ingestion in the world. Because overdose of APAP has life-threatening effects on kidney, treatment of APAP-induced nephrotoxicity has life-saving importance. Aim of the study was to evaluate the efficacy of medical ozone therapy in experimental model of APAP toxication. Twenty-one male Wistar rats (200-250 g) were randomly assigned into three groups containing seven rats each: Sham, control (only APAP treated), and APAP + ozone therapy groups. Rats were killed 48 hours after administration of APAP. Urea, creatinine levels in the blood, and malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activity in renal tissue were measured. Kidney tissues were stained with hematoxylin and eosin for histological assessment. APAP administration deteriorated the renal functions and significantly elevated renal MDA levels and depleted SOD and GSH-Px activities. Ozone therapy significantly reduced the MDA level, increased the SOD and GSH-Px activities, and normalized the renal histology. In conclusion, our study results are consistent with encouraging data for ozone therapy on APAP-induced nephrotoxicity in rats by improving antioxidant mechanism and oxidative stress.

The efficacy of ozone therapy in experimental caustic esophageal burn.

INTRODUCTION: Ozone has been proposed as an antioxidant enzyme activator, immunomodulator and cellular metabolic activator. This study was designed to investigate the efficacy of ozone therapy in the prevention of esophageal damage and stricture formation developed after esophageal caustic injuries in the rat. MATERIALS AND METHODS: Forty-five rats were allocated into three groups; sham-operated, un-treatment and treatment groups. Caustic esophageal burn was created by instilling 15% NaOH in the distal esophagus. The rats were left untreated or treated with 1 mg/kg/day ozone intraperitoneally. All rats were sacrificed at 28 days. Efficacy of the treatment was assessed by measuring the stenosis index (SI) and histopathologic damage score, and biochemically by determining tissue hydroxyproline content (HP), superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA) and protein carbonyl content (PCC) in esophageal homogenates. RESULTS: Whereas seven (47%) rats died in the un-treatment group, all rats in the sham-operated and the treatment group survived during the study. SI, the histopathologic damage score, was significantly lower in the ozone-therapy group than the un-treatment group. HP levels were significantly higher in the un-treatment group than the group treated with ozone. Caustic esophageal burn increased MDA and PCC levels and also decreased SOD and GPx enzyme activities. In contrast, ozone therapy decreased the elevated MDA and PCC levels and also increased the reduced SOD and GPx enzyme activities. CONCLUSION: Ozone has a preventive effect in the development of fibrosis by decreasing tissue damage and increasing the antioxidant enzyme activity in an experimental model of corrosive esophageal injury.

Bronchial tear in a child after a liquid petroleum gas tank explosion.

Humans have been exposed to blast effects since the invention of gunpowder and explosives. Bronchial injury because of an explosion is a rare but lethal injury that requires prompt recognition and treatment. In this article, we present a case of a bronchial tear after an explosion.