We evaluated the efficacy of hyperbaric oxygen (HBO2) therapy used as a supplement to the first-line medical treatment of sudden sensorineural hearing loss (SSNHL). We tested 68 patients suffering from SSNHL within seven days of hearing loss: 21 patients received the standard treatment protocol of our department (control group) and 47 individuals were treated with an additional application of HBO2 therapy. Treatment success was assessed using pre- and post-treatment audiograms. Outcomes of our study showed a statistically significant improvement in auditory threshold in all frequency groups for the HBO2 group (P < 0.001), whereas in the control group the statistically significant mean auditory gain was observed only for the frequency zone 1,000 to 2,000 Hertz (P = 0.01). Furthermore, the rate of hearing gain in the HBO2 group was more than doubled (61.7%) compared to the control group (28.6%). Complete recovery of the hearing gain in the control group was observed only in the first two frequency groups (14.29%; 4.76%; 0.00%), whereas in the HBO2 group complete recovery was seen in all the frequency groups (19.15%; 21.13%; 6.38%) as well as in the whole frequency range (6.38%). The efficiency of both treatment protocols was statistically significant (P < 0.001) in both groups of patients, but supplementation of the therapy with HBO2 demonstrated a statistically significantly increase in the effect of pharmacotherapy (P < 0.001) by 11.5 decibels (dB) up to the final hearing gain of 20 dB. HBO2 is therefore a promising modality of SSNHL treatment, but specific mechanisms of HBO2 in patients with SSNHL arestill unknown. Further investigations are warranted to explore the mechanisms of action.

Nature is an attractive source of therapeutic compounds. In comparison to the artificial drugs, natural compounds cause less adverse side effects and are suitable for current molecularly oriented approaches to drug development and their mutual combining. Medicinal plants represent one of the most available remedy against various diseases. Proper examples are Salvia officinalis L. and Thymus vulgaris L. which are known aromatic medicinal plants. They are very popular and frequently used in many countries. The molecular mechanism of their biological activity has not yet been fully understood. The aim of this study was to ascertain if liver cells of experimental animals drinking extracts of sage or thyme will manifest increased resistance against oxidative stress. Adult Sprague-Dawley rats were divided into seven groups. They drank sage or thyme extracts for 2 weeks. At the end of the drinking period, blood samples were collected for determination of liver biochemical parameters and hepatocytes were isolated to analyze (i) oxidatively generated DNA damage (conventional and modified comet assay), (ii) activities of antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GPx)] and (iii) content of glutathione. Intake of sage and thyme had no effect either on the basal level of DNA damage or on the activity of SOD in rat hepatocytes and did not change the biochemical parameters of blood plasma. Simultaneously, the activity of GPx was significantly increased and the level of DNA damage induced by oxidants was decreased. Moreover, sage extract was able to start up the antioxidant protection expressed by increased content of glutathione. Our results indicate that the consumption of S.officinalis and T.vulgaris extracts positively affects resistency of rat liver cells against oxidative stress and may have hepatoprotective potential.

Lavender is a commonly used herb in traditional medicine in Asia and Europe. It has been reported to be an effective medical plant in treating inflammation, depression and stress, thanks to its sedative and anxiolytic action, thrombotic, and antimicrobial properties. In the present study we investigated the protective effects of essential oil from Lavandula angustifolia (LO) against hydrogen peroxide and tert-butyl hydroperoxide -induced DNA damage. Also the effects of LO on the levels of enzymatic and non-enzymatic antioxidants (SOD-superoxide dismutase, GPx-glutathione peroxidase, GSH-glutathione) were evaluated in in vitro (human hepatoma cell line HepG2) and in ex vivo (freshly isolated rat hepatocytes) systems. The results showed that the oxidant-induced DNA lesions were significantly reduced in both systems pre-treated with the Lavandula angustifolia. The observed DNA-protective activity could be explained by both elevation of GPx activity in cells pre-treated with LO and antioxidant activity of LO.

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Because genetic predisposition to atherothrombosis in systemic lupus erythematosus (SLE) remains to be determined, the most common genetic prothrombotic factors, prothrombin G20210A and factor V Leiden mutations, were studied. Seventy-four SLE patients with vascular ischemia (SLE cases) were studied and stratified into myocardial infarction and/or cerebrovascular accident subgroup (MI/CVA), and coronary heart disease subgroup without overt arterial thrombotic events (CHD). Seventy-one SLE patients without atherothrombosis were investigated as SLE controls. Factor V Leiden was detected in six cases (five in MI/CVA, one in CHD group) and three controls (OR 2.00, 95%CI 0.48-8.32). Two cases (both CHD patients) had prothrombin G20210A mutation vs. three controls (OR 0.63, 95%CI 0.1-3.88). Anticardiolipin antibodies (aCL) were increased in cases vs. controls (39/74 vs. 27/71); however, this was not statistically significant (OR 1.82, 95%CI 0.94-3.52). Neither univariate nor multivariate analysis indicated that investigated mutations are risk factors for atherothrombosis in SLE cases, MI/CVA, or CHD subgroups. Overall, disease activity was the strongest risk factor for atherothrombosis (p=0.0014) in SLE cases. Combination of disease activity+gender was the best predictor of atherothrombotic process (p=0.00045) in this cohort. In MI/CVA subgroup, disease activity was the only predictor (p=0.0058). In CHD patients, the best predictive value was conferred by combination of hypertension+gender+disease activity (p=0.00077). No other investigated risk factor (including aCL) conferred an increased risk individually or potentiated the other risk factors. The results deny the role of investigated mutations in atherothrombosis in SLE, but they underscore the importance of disease activity (i.e., ongoing inflammation) in pathogenesis of atherosclerosis and arterial thrombosis.