Erythrocyte osmotic fragility and lipid peroxidation in experimental hyperthyroidism.

This study investigated the relation between erythrocyte osmotic fragility and oxidative stress and antioxidant state in primary hyperthyroidism induced experimental rats. Twenty-four Spraque-Dawley-type female rats weighing between 160 and 200 g were divided into two, as control (n = 10) and experimental (n = 12), groups. The experimental group animals have received tap water and L-Tiroksin (0.4 mg/100 g fodder) added standard fodder for 30 days to induce hyperthyroidism. Control group animals were fed tap water and standard fodder for the same period. Blood samples were drawn from the abdominal aorta of the rats under ether anesthesia. T3, T4, and TSH levels, osmotic fragility, malondialdehyde (MDA), superoxide dismutase, and glutathione levels were measured in the blood. There was a statistically significant deviation found in maximum and minimum osmotic hemolysis limit values of experimental group when compared to controls. The standard hemolytic increment curve of the hyperthyroid group shifted to the right when compared to control group's curve. There was a statistically significant increase found in MDA and superoxide dismutase, but statistically a significant decrease was detected in glutathione levels in hyperthyroid group when compared to controls. As a result of our study, it may be concluded that hyperthyroidism may led to an increase in osmotic fragility of erythrocytes and this situation may possibly originate from the increased lipid peroxidation in hyperthyroidism.

The effect of heme oxygenase-1 induction by octreotide on radiation enteritis.

Radiation enteritis occurs as a response to abdominal radiation, which can cause mucosal damage in the gastrointestinal mucosal epithelium. The small intestine is one of the most radiosensitive organs in the abdomen. The present study was undertaken to investigate the effect of octreotide (OCT) administration on heme oxygenase-1 (HO-1) expression of the radiation enteritis model. Rats received 50 mg/kg/day OCT for 4 days before irradiation and continued for 3 days after irradiation. Intestinal myeloperoxidase (MPO) activities, malondialdehyde (MDA) levels are indicators of oxidative damage while caspase-3 activities reveal apoptosis degree of the small intestine. At histological examination, the terminal ileum tissue was analyzed for morphological changes. Irradiation significantly increased the intestinal MPO and caspase-3 activities, MDA levels and HO-1 expression in comparison to sham control group. OCT treatment was associated with increased HO-1 expression and caspase-3 activity, decreased MPO activity and MDA levels. Histological examination revealed that the intestinal mucosal structure was preserved in the OCT treated group. OCT appears to have protective effects against radiation-induced intestinal damage. This protective effect is, in part, mediated by modification of the inflammatory response and the induction of HO-1 expression.

Bone metabolism in ovariectomized rats with induced hyperthyroidism: the effect of estrogen replacement.

We aimed to investigate whether or not the estrogen is playing any role in the effect of thyroid hormones on bone metabolism. The rats were divided into five groups. In the first group L-thyroxine-induced hyperthyroid rats were ovariectomized (OVX) while the OVX rats were administered L-thyroxine in the second group. 17beta-Estradiol (E2) was replaced in OVX rats in Group III. L-thyroxine and E2 were simultaneously administered to OVX rats in Group IV. The fifth group received sham operation. Blood samples taken from the tail vein of rats were analyzed for plasma T3, T4, TSH and serum interleukin (IL)-1beta, IL-6, tumor necrosis factor (TNF)alpha, calcium (Ca), phosphorous (P), parathyroid [corrected] hormone (PTH), alkaline phosphatase (t-ALP), bone-specific alkaline phosphatase (b-ALP) and E2. The levels of cytokines, t-ALP and b-ALP increased but PTH decreased, while there was no change in Ca and P levels in L-thyroxine-administrated rats. However, the levels of cytokines, Ca, P, PTH, t-ALP and b-ALP did not change in L-thyroxine-administered OVX rats. In OVX rats, the cytokines, t-ALP and b-ALP increased while Ca, P remained the same, but PTH decreased. L-thyroxine administration to OVX rats did not change the cytokines, Ca, P, PTH, t-ALP and b-ALP levels. The replacement of E2 in OVX rats decreased the cytokines, t-ALP and b-ALP values, increased PTH levels while there was no change in Ca and P. L-thyroxine and E2 administration to OVX rats increased the cytokines, t-ALP and b-ALP levels and decreased PTH, but Ca and P remained the same. In sham-operated rats, there was no change in all parameters compared to initial values. This study suggests that estrogen may play a role in the effects of thyroid hormones on bone metabolism.

Effects of flurbiprofen and tiaprofenic Acid on oxidative stress markers in osteoarthritis: A prospective, randomized, open-label, active- and placebo-controlled trial.

BACKGROUND: The relationship between oxidative stress and osteoarthritis (OA) has been widely investigated. Serum malondialdehyde (MDA), nitric oxide (NO), and Cu/Zn superoxide dismutase (SOD) levels are useful markers of oxidative stress. Because of the importance of oxidative stress markers in the pathogenesis of OA, treatment might involve modification of these markers to control oxidative stress. OBJECTIVE: The aim of this study was to compare the effects of 2 conventionalNSAIDs on markers of oxidative stress in patients with OA of the knee. METHODS: This 3-week, prospective, randomized, open-label, active- and placebo-controlled study was conducted at the Cerrahpasa Faculty of Medicine, Istanbul University, Istanbul, Turkey. Adult patients with clinically and radiographically diagnosed moderate OA of the knee who were previously untreated were enrolled. Patients were randomly assigned to 1 of 3 treatment groups: flurbiprofen 100 mg PO (tablets) BID, tiaprofenic acid 300 mg PO (tablets) BID, or placebo tablets BID. Patients were evaluated using clinical assessment and laboratory testing before treatment (week 0; baseline) and at the end of week 3. The primary end points were the differences in serum MDA, NO, and SOD levels versus placebo. Clinical parameters-pain at rest and on motion-were evaluated using a 10-cm visual analog scale (0 = no pain to 10 = worst pain imaginable). The duration (in minutes) of morning stiffness was recorded by patients, using patient diaries. The differences between treatment groups were assessed using multivariate analysis. RESULTS: Thirty-nine patients (20 women, 19 men; mean [SD] age, 59.0 [11.3]years) were included in the study. Mean serum MDA and NO levels were significantly decreased at 3 weeks compared with baseline in the 2 active-treatment groups (all, P < 0.001); these values remained statistically similar to baseline in the placebo group. Serum SOD levels were increased significantly from baseline in the 2 active-treatment groups (both, P < 0.001), but not in the placebo group. No significant differences in serum MDA and NO levels were found between the group receiving flurbiprofen and that receiving tiaprofenic acid. Serum SOD levels were significantly higher in the flurbiprofen group compared with the tiaprofenic acid and placebo groups (both, P < 0.01). The mean (SD) score for pain at rest was significantly lower at 3 weeks compared with baseline with flurbiprofen and tiaprofenic acid (both, P < 0.001), but not with placebo. The mean score for pain on motion was significantly reduced from baseline values only with tiaprofenic acid (P < 0.001). The duration of morning stiffness was significantly shorter at 3 weeks compared with baseline in all 3 study groups (all, P < 0.001). The mean scores for pain on motion and duration of morning stiffness were significantly reduced with tiaprofenic acid compared with placebo (both, P < 0.05). The study had some limitations (ie, small sample size, no blinding, the short duration of the study, and the weak correlation between serum and synovial fluid levels of NO). CONCLUSIONS: In this comparison of the effects of 3 weeks of treatment withflurbiprofen 100 mg BID and tiaprofenic acid 300 mg BID in patients with knee OA, both treatments effectively reduced serum MDA and NO levels compared with placebo. Only tiaprofenic acid significantly improved pain at rest and on motion and duration of morning stiffness compared with placebo.