DNA integrity in patients undergoing hyperbaric oxygen (HBO) therapy.

Hyperbaric oxygen (HBO) therapy is successfully applied for a wide variety of diseases. However, recent studies in humans undergoing (HBO) therapy have revealed that HBO is able to induce oxidative DNA damage especially in lymphocytes while the biological significance of this outcome is still not clear. HBO mediated DNA damage in lymphocytes has been determined by using the alkaline version of the comet assay in order to detect DNA strand breakages in patients undergoing HBO therapy. Blood samples were obtained from 100 voluntary patients and were drawn by venipuncture before and immediately after the first session of HBO treatment. The DNA damaging effect of HBO has also been evaluated in the fifth session of HBO therapy. DNA strand breakages were significantly increased after the first session of HBO treatment. However the elevated DNA strand breaks returned to their normal levels in lymphocytes after two hours of in vitro incubation. The elevated DNA strand breaks consistently decreased and reached to the baseline levels after the fifth session of HBO therapy. The results of this study, conducted in patients undergoing HBO therapy, support the existence of the previously reported cellular adaptive response against HBO mediated oxidative DNA damage in experimental studies.

Time-dependent course of hyperbaric oxygen-induced oxidative effects in rat lung and erythrocytes.

1. The oxygen toxicity of hyperbaric oxygen (HBO) treatment has long been of interest. There is an extensive amount of information regarding the role oxidative stress plays after HBO exposure in different tissues, but the question of the persistence of this oxidative effect has not been thoroughly elucidated. 2. The present study was performed to elucidate the persistence of the oxidative effects of HBO on rat lungs and erythrocytes after they had been subjected to 100% oxygen exposure. 3. Rats were divided into five groups. All animals, except those in the control group, were subjected to 100% oxygen for 2 h at 3 ATA ( identical with 300 kPa). Rats were killed at 30, 60, 90 or 120 min after exposure and thiobarbituric acid-reactive substances (TBARS) levels and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were determined. 4. Thiobarbituric acid-reactive substances levels and SOD and GPx levels were found to be significantly increased in lung tissue up to 60 min after exposure. Superoxide dismutase activity persisted at significantly high values for 90 min after exposure in erythrocytes and the lung. The TBARS levels in erythrocytes were also significantly higher for 60 min, whereas increased GPx activity was observed to persist for only 30 min. 5. The oxidative effect of HBO exposure declines to physiological levels within 90 min at most for erythrocytes and in lung tissue in rats. Further studies should focus on the molecular mechanisms that can be activated during this time interval.

Persistence of hyperbaric oxygen-induced oxidative effects after exposure in rat brain cortex tissue.

Hyperbaric oxygen (HBO) causes oxidative stress in several organs and tissues. Due to its high rate of blood flow and oxygen consumption, the brain is one of the most sensitive organs to this effect. Many studies have reported oxidative effects of HBO, but there is no comprehensive data about how long this effect persists. The aim of this study was to elucidate the duration of HBO-induced oxidative/antioxidant action. Male Sprague-Dawley rats were divided into 5 groups. Except for the controls, the animals were subjected to 100% oxygen for 2 h at 3 atm and differed from each other by the time to dissection after exposure that began at 30, 60, 90, or 120 min. Thiobarbituric acid-reactive substances (TBARS), as well as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity was determined in brain cortex tissue. Additionally, nitrite-nitrate (NO(x)) concentrations were measured. All measured parameters were found to be significantly increased 30 min after exposure. SOD and GSH-Px levels persisted at significantly high levels for 60 min. In conclusion, the oxidative effect of HBO was shown to persist only for 1 h. Further studies should be performed to elucidate the possible molecular interactions during this period.

Effectiveness of hyperbaric oxygen on sudden sensorineural hearing loss: prospective clinical research.

The role of hyperbaric oxygen (HBO) treatment in sudden sensorineural hearing loss (SSNHL) is still controversial. In this study, 80 patients were treated for SSNHL. Fifty-five patients who received HBO and medical treatment and 25 patients who received medical treatment only were studied. There was a statistically significant difference between the HBO and medical treatment group and the medical treatment group for hearing gain and the degree of hearing loss after treatment (p<.05). In the HBO and medical treatment group, patients with tinnitus showed the highest hearing improvement. The patients who had tinnitus had a statistically significant difference for hearing gain in the HBO and medical treatment group (p<.05) but not in the medical treatment group (p>.05). In the HBO and medical treatment group, average hearing gain on each audiometric frequency was better than in the medical treatment group (p<.05).

Increased sensitivity to mitomycin C-induced sister chromatid exchange in lymphocytes from patients undergoing hyperbaric oxygen therapy.

Treatment of cells with hyperbaric oxygen (HBO) results in the generation of reactive oxygen species and the induction of DNA damage. In the present study, we have evaluated the sister chromatid exchange (SCE) frequencies in lymphocytes from patients undergoing hyperbaric oxygen therapy (HBOT). In addition, we have determined the sensitivity of lymphocytes from those patients to SCE induction by 20 and 40 ng/ml mitomycin C (MMC). Patients undergoing HBOT for diabetic feet were exposed to 10 consecutive daily HBO treatments according to a routine therapy protocol. The study began with 12 patients; however, it was not possible to sample all of the patients at all HBOT sessions, and the number of patients gradually decreased towards the end of the HBOT. We observed a statistically significant induction in mean SCE/cell (P < 0.05; n = 11) immediately after the first session of HBOT. Relative to its frequency after the 1st treatment, the mean SCE frequency gradually decreased after the 5th and 10th HBOT sessions and reached baseline (pretherapy) levels 1 day after the last treatment in the four patients that were sampled. The mean MMC-induced SCE frequency was highest in lymphocytes sampled immediately after the first HBOT session, and significantly higher than the MMC-induced SCE frequency in cells sampled before HBOT. Unlike the case with untreated cells, MMC-induced SCE frequencies remained high in lymphocytes sampled at later stages of therapy and mean MMC-induced SCE frequencies were significantly higher (P < 0.05; n = 4) in lymphocytes sampled 1 day after the last session of HBOT than in lymphocytes sampled from these patients prior to beginning the therapy. The results indicate that HBOT induces SCE and that lymphocytes retain increased sensitivity to the genotoxicity of MMC one day after completing the HBOT.

The effects of hyperbaric oxygen treatment on oxidative stress and SCE frequencies in humans.

OBJECTIVES: Hyperbaric oxygen (HBO) therapy is a useful method for treatment of various clinical conditions but it can also cause an increased production of free radicals and oxidative DNA damage. In this study, our aim was to investigate the effects of hyperbaric oxygen on oxidative stress and genetic toxicity. DESIGN AND METHODS: Fifteen patients were exposed to HBO treatment for various pathologies related to hypoxia. Blood samples were taken before HBO therapy and at the end of the 1st, 10th and 20th HBO sessions. Antioxidant parameters and genetic toxicity were studied. RESULTS: We have observed that an increment of lymphocyte sister chromatid exchange (SCE) frequency was detected at the end of the 1st, 10th and 20th HBO sessions compared to before HBO treatment (P<0.05). No significant difference in erythrocyte copper-zinc superoxide dismutase (CuZn-SOD), selenium dependent glutathione peroxidase (SeGSH-Px) and malondialdehyde (MDA) levels were observed at the end of the 1st HBO therapy and the prolonged HBO exposure as compared to before HBO treatment (P>0.05). CONCLUSIONS: Our results indicate that HBO treatment did not cause significant changes on erythrocyte antioxidant capacity and lipid peroxidation; however, it could induce genotoxicity due to different mechanisms.

Beneficial effect of hyperbaric oxygenation on liver regeneration in cirrhosis.

BACKGROUND: Underlying hepatic injury and cirrhosis are leading factors that interfere with the post-operative liver regeneration and function. Hyperbaric oxygenation (HBO) has been reported to ameliorate the ischemia-reperfusion injury of the liver, to induce compensatory hypertrophy of the predicted remnant liver in rats after portal vein ligation and to augment liver regeneration after hepatectomy in non-cirrhotic rats. Our aim was to determine the effect of HBO treatment on liver regeneration after partial hepatectomy in normal and cirrhotic mice in this experimental study. MATERIALS AND METHODS: The effect of HBO on liver regeneration was studied in a mice model combining carbon tetrachloride induced cirrhosis and partial hepatectomy. Mice were divided into four groups: Control, cirrhotic, non-cirrhotic HBO-treated, and cirrhotic HBO-treated. All animals underwent 40% hepatectomy. Liver regeneration was evaluated by the proliferating cell nuclear antigen-labeling index. Serum aspartate aminotransferase and alanine aminotransferase levels were measured to evaluate liver injury. RESULTS: Serum alanine aminotransferase and aspartate aminotransferase levels were significantly decreased in HBO-treated cirrhotic group compared to cirrhosis group after hepatectomy (P = 0.001 and P = 0.014, respectively). The proliferating cell nuclear antigen labeling index was significantly higher in HBO treated cirrhotic group than in cirrhotic group after hepatectomy (P = 0.022). CONCLUSIONS: Our results suggest that HBO treatment improves liver functions and augments hepatocyte regeneration in cirrhotic mice after hepatectomy. Post-operative HBO treatment may have a beneficial effect on post-operative liver function and regeneration in cirrhotic patients.

Maggot debridement therapy in the treatment of chronic wounds in a military hospital setup in Turkey.

BACKGROUND: The medicinal use of maggots for the biological debridement of chronic wounds is increasing around the world, due to its efficacy, safety and simplicity. Thousands of patients have been treated in private and governmental hospitals during the last 10 years. OBJECTIVE: To examine the efficacy of maggot debridement therapy (MDT) in the debridement of chronic wounds in a military hospital. METHODS: MDT was applied for 1-9 days to 7 male and 4 female soldiers or their family members (21-72 years old) with chronic wounds. RESULTS: Complete debridement was achieved in 10 out of 11 patients, while in 1 patient the wound could be cleaned only partially. A remarkable reduction in the odor emanating from the wound and notable granulation were observed in all debrided wounds. Increased pain was observed in 1 patient with a venous stasis ulcer. CONCLUSION: We believe that MDT is a rapid and effective method for the debridement of chronic wounds in a military environment especially in times of war in developing countries.

Protective effects of exogenously administered or endogenously produced melatonin on hyperbaric oxygen-induced oxidative stress in the rat brain.

1. Hyperbaric oxygen (HBO) is a widely used treatment modality in many diseases. A known side-effect of HBO is the production of reactive oxygen species (ROS). Many anti-oxidants, such as vitamins C and E, riboflavin and selenium, have been used successfully to scavenge the ROS produced by HBO administration. 2. The aim of the present study was to determine whether melatonin, a newly discovered anti-oxidant, has a protective effect against the overproduction of ROS produced by HBO in rat brain tissue. 3. Seventy male Sprague-Dawley rats were divided into seven groups as follows: 1, daytime control; 2, daytime HBO; 3, melatonin; 4, daytime HBO plus melatonin; 5, night-time control; 6, night-time HBO; and 7, night-time HBO under light exposure. 4. Hyperbaric oxygen was administered at 303 kPa for 120 min. Melatonin was injected at a dose of 10 mg/kg, i.p. Brain malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels were measured to elucidate oxidant status. 4. The MDA and SOD levels of groups 2 and 7 increased significantly. Exogenous (group 4) and endogenous (group 6) melatonin protected against HBO-induced lipid peroxidation. Exogenously administered melatonin (groups 3 and 4) had increased levels of the anti-oxidant enzymes SOD and GPx. 5. In conclusion, HBO caused oxidative stress and melatonin exhibited protective effects. Both endogenously produced and exogenously administered melatonin were found to be effective.

Acute arterial thrombotic purpura complicating varicella and the role of hyperbaric oxygen as an adjunctive therapy.

Chickenpox is a common infectious disease of the pediatric age group with rare complications such as hemorrhagic varicella and arterial thrombotic purpura. Medical support is the mainstay of treatment in such cases but for the rescue of necrotic tissues, hyperbaric oxygen (HBO) therapy should be applied in addition to anticoagulant intervention. We report an infant with acute arterial thrombotic purpura which developed after varicella eruption and who made full recovery with the help of HBO as an adjunctive treatment modality. Fresh frozen plasma and low molecular weight heparin were given for prolonged prothrombin time and thromboemboli on the 2nd-4th digits of his right foot. Protein C, protein S and factor V levels were found to be normal in our patient. Necrotic lesions on the toes regressed with repeated HBO treatment and amputation was not needed.

Hyperbaric oxygen prevents bacterial translocation in thermally injured rats.

This study was designed to evaluate the effects of hyperbaric oxygen (HBO2) on intestinal microflora and bacterial translocation (BT) caused by experimentally induced thermal injury in rats. Rats were separated into four groups, namely, HBO2 group, thermal injury (TI) group, TI + HBO2 group, and control group. All groups were further separated into short-term (2 days) and long-term (7 days) treatment or injury groups. Control group was neither exposed to thermal injury nor was given any treatment. Thirty percent second-degree thermal burn was induced on the dorsal body part of the rats in TI groups. In the HBO2 groups, rats received HBO2 treatment either without TI or following TI induction, for 2 and 7 days, respectively. Sampling from tissues and portal vein was performed on day 3 in the short-term groups and on day 8 in the long-term groups. Samples were cultured for identification of bacteria and colony counts. HBO2 treatment significantly reduced the colony counts of endogenous microflora in distal ileum of healthy rats (p < .05), while TI significantly increased the colony counts of endogenous microflora in distal ileum in short and long-term TI groups (p < .05). Presence of bacterial translocation was proven by bacterial isolation in mesenteric lymph nodes, liver, spleen and blood. Both short- and long-term HBO2 treatment following TI significantly reduced the colony counts of intestinal microflora (p < .05) and prevented bacterial translocation almost completely. It is concluded that thermal injury causes both bacterial overgrowth within intestinal lumen and bacterial translocation across the intestinal wall. HBO2 administration prevents both bacterial overgrowth and translocation.