Purpose To establish the effect of systemic oxidative stress on the pathogenesis of keratoconus by measuring serum total oxidant status (TOS) and total antioxidant status (TAS) in patients with keratoconus. Methods Twenty-five patients with keratoconus (keratoconus group) and 25 age-sex-matched healthy subjects (control group) were enrolled in the study. Exclusion criteria were smoking habit, history of any other corneal pathology, systemic disease or inflammation, and current antioxidant or anti-inflammatory therapies. All participants underwent a detailed ophthalmological examination and corneal topography. Serum samples were obtained from all participants. Oxidative stress markers (TAS and TOS) were measured using a commercial kit and oxidative stress index (OSI) was calculated. Results The study comprised 25 patients with keratoconus (mean age of 26.4 ± 1.7 years) and 25 healthy control subjects (mean age of 26.6 ± 1.7 years) (P40.05). The serum TOS and OSI values were significantly higher in patients with keratoconus compared with those of the controls (P ¼ 0.036 and 0.037, respectively). However, serum TAS did not show significant difference between the keratoconus and control groups (P ¼ 0.497). Conclusions The higher levels of serum oxidant status and OSI in patients with keratoconus suggest that systemic oxidative stress might be involved in the pathogenesis of keratoconus.

SummaryBackgroundThis study aimed to explore the effects of progressive resistance exercise training (PRET) on hemorheology.Material/MethodsExercise sessions included 1–3 sets of 8–12 repetitions at 40–60% of 1-repetition maximum (1-RM) for 3 weeks and at 75–80% of 1-RM during weeks 4–12. Red blood cell (RBC) deformability and aggregation were determined by ektacytometry, plasma and whole blood viscosities (WBV) by rotational viscometry. Lactate concentration was evaluated by an analyzer and fibrinogen was evaluated by coagulometry. Plasma total oxidant/antioxidant status was measured by colorimetry.ResultsFollowing an acute increase after exercise on the first day, RBC deformability was elevated during weeks 3 and 4 (p=0.028; p=0.034, respectively). The last exercise protocol applied in week 12 again caused an acute increase in this parameter (p=0.034). RBC aggregation was increased acutely on the first day, but decreased after that throughout the protocol (p<0.05). At weeks 4 and 12 pre-exercise measurements of WBV at standard hematocrit and plasma viscosity were decreased (p=0.05; p=0.041, respectively), while post-exercise values were increased (p=0.005; p=0.04, respectively). Post-exercise WBV at autologous hematocrit measured at week 12 was increased (p=0.01). Lactate was elevated after each exercise session (p<0.05). Fibrinogen was decreased on the third week (p<0.01), while it was increased on the 4th week (p=0.005). Plasma antioxidant status was increased at week 3 (p=0.034) and oxidative stress index was decreased at week 4 (p=0.013) after exercise.ConclusionsThe results of this study indicate that PRET may have positive effects on hemorheological parameters.

The SCFP is associated with increased RBC deformability and decreased RBC aggregation. These hemorheological alterations, possibly also contributing factors in limiting the pathogenesis, can especially serve as beneficial adaptive mechanisms in the SCFP.

This study aimed to investigate the effects of moderate intensity swimming exercise (10 weeks) followed by detraining (for five and 10 weeks) on oxidative stress levels of heart, lung, kidney, and liver tissues and systolic blood pressure (SBP) of spontaneously hypertensive rats (SHR). SHR and control rats were randomized into sedentary, exercised, detrained (5 weeks) and late-detrained (10 weeks) groups. Corresponding sedentary rats were grouped as time 1-2-3. Exercise of 60 min, 5 days/week/10 weeks was applied. Detraining rats underwent the same training protocol and then discontinued training during next 5, 10 weeks. SBP was measured by tail-cuff method. Tissue total oxidant/antioxidant status was measured using a commercial kit and oxidative stress index (OSI) was calculated. Exercise training slightly decreased tissue OSI of SHR and reduced SBP of both groups. Tissue OSI of SHR were higher than WKY and aging resulted in increment of oxidants in groups. detraining yielded time-dependent increments in oxidative stress of all tissues and SBP of both rat groups. Although short-term cessations may be tolerated, our results emphasize the importance of exercising as a way of life for cardiovascular well-being in hypertensives or in individuals who are genetically under risk of hypertension.

No abstract