Mukaddes Canbaz

Antioxidant defence in recurrent abortion

Increased free radical activity has been implicated in the pathogenesis of recurrent abortion. This investigation was conducted to determine if changes in some parameters of the antioxidant system contribute to this condition. Plasma ascorbic acid, alpha-tocopherol, total thiols, ceruloplasmin, uric acid, albumin, and erythrocyte glutathione (GSH) were assayed in 25 nonpregnant (NP) healthy women, 25 normotensive pregnants (NTP), and 120 women with recurrent abortion. Recurrent aborters were divided into four subgroups according to the etiology: autoimmune (AUTO, n=25), luteal phase defect (LPD, n=25), anatomical defect (AD, n=20) and unexplained (UNEx, n=50). Plasma levels of ascorbic acid, alpha-tocopherol, and erythrocyte GSH were significantly decreased in AUTO, UNEx and LPD subgroups than those in two control groups and the AD group (ANOVA). Plasma thiols of UNEx and AUTO aborters were diminished according to controls and other abortion subgroups (ANOVA). Ceruloplasmin levels showed a decline in AUTO and UNEx subgroups when compared to controls, AD and LPD aborters (ANOVA). When UNEx, AUTO and LPD recurrent abortion subgroups were compared with each other (Students t-test) total thiols and erythrocyte GSH of UNEx and AUTO subgroups were diminished in comparison with LPD. We suggest that decreased concentrations of plasma ascorbic acid, alpha-tocopherol, total thiols and erythrocyte GSH in UNEx, AUTO and LPD reflect the increased oxidative stress, expressing a progress of the condition. Also, the imbalance between antioxidant defence and free radical activity is more evident in the AUTO subgroup. As a conclusion, although impaired antioxidant defence may be responsible for recurrent abortions, the recurrent abortions may also result in oxidative stress and depletion and weakness of antioxidant defence.

Plasma antioxidant defense in actinic keratosis and basal cell carcinoma

Reactive oxygen species and lipid peroxides have been implicated in the pathogenesis of a variety of diseases, particularly cancer. There may be an inverse correlation between lipid peroxidation and antioxidant defense mechanisms. The aim of this study was to investigate whether certain plasma antioxidants (ascorbic acid, α‐tocopherol, total thiol groups, ceruloplasmin, urate, albumin and erythrocyte glutathione) are altered in actinic keratosis (AK) and basal cell carcinoma (BCC).

Effects of menopause and tibolone on antioxidants in postmenopausal women

Background: Oxidative stress has been implicated in the pathogenesis of ageing and menopause, and can arise through the increased production of lipid peroxides and/or a deficiency of antioxidant defence. Aim: To investigate the effects of the menopause and tibolone treatment (2.5 mg/day for six months) on plasma antioxidants and lipid peroxidation. Methods: Plasma concentrations of ascorbic acid, α-tocopherol, total thiol groups, caeruloplasmin, erythrocyte glutathione (GSH) and malondialdehyde (MDA) were measured in 24 postmenopausal and 24 premenopausal healthy women. Results: Data analysis indicates a significant decrease in plasma ascorbic acid, α-tocopherol, total thiol groups, caeruloplasmin, erythrocyte GSH and a significant increase in lipid peroxides (expressed as MDA concentrations) in postmenopausal women. There was no significant difference between control and study groups in the mean plasma caeruloplasmin concentrations. It was found that there is a significant increase in α-tocopherol and significant decrease in lipid peroxide concentrations in postmenopausal after tibolone treatment. Conclusions: The menopause is associated with an increase in oxidative stress and a decrease of some antioxidants, such as ascorbic acid, α-tocopherol, total thiols and erythrocyte GSH. Tibolone treatment leads to a decrease in concentrations of plasma lipid peroxide, probably by stimulating direct and indirect mechanisms of tocopherol regeneration and increasing plasma concentrations of vitamin E. However, due to the relatively small numbers involved this study can be regarded as a pilot. Further studies performed on a larger scale are necessary to establish the exact mechanisms of tibolone in inhibiting oxidative stress in postmenopausal women.

Nitric oxide and endothelin-1,2 in actinic keratosis and basal cell carcinoma: changes in nitric oxide/endothelin ratio.

Abstract

Effects of diabetes mellitus and acute hypertension on plasma nitric oxide and endothelin concentrations in rats

AIM To examine the plasma nitrate/nitrite (NOx-two end products of the nitric oxide metabolism) and endothelin (ET) concentrations, and response to acute adrenaline induced hypertension in diabetic rats. MATERIALS AND METHODS Four groups of 4-month-old rats were used: control rats (C, n=10) rats received adrenaline (A, 40 microg/kg i.v., n=10), rats received streptozotocin (S, 50 mg/kg i.v., n=8), and rats received STZ and adrenaline (SA, n=9). The experiments were performed 4 weeks after the STZ administration. Plasma NOx, ET, glucose, and mean arterial blood pressure (MAP) were measured. RESULTS Plasma ET concentrations were significantly increased in diabetic rats (S and SA) in comparison with the controls and adrenaline-only administered rats. NOx concentrations in diabetic groups (S and SA) were significantly decreased in comparison with the controls. Acute adrenaline induced hypertension in diabetes leads to a significant decrease of NOx concentrations in comparison with the controls, adrenaline-only administered and STZ-only administered rats. There was no difference between the MAP in diabetic and control rats. Adrenaline injection caused a significant increase of MAP in A and SA groups. Plasma glucose concentrations in diabetic rats (S and SA) were significantly increased in comparison with the nondiabetic groups (C and A). There was a weak but significant correlation between the NOx and ET concentrations in the controls, which probably reveal the balance between these vasoactive factors. In A, S, and SA groups, no significant correlation between the NOx/ET was found. CONCLUSION An impairment of the NOx and ET formation could be involved in the pathogenesis of diabetes mellitus and especially acute hypertension and diabetes. A lack of correlation between the NOx and ET probably indicated that in diabetes and acute hypertension, a primary mechanism of compensatory nitric oxide might be lost.

Hormone replacement therapy and urinary prostaglandins in postmenopausal women

The objective of the study was to observe the effects of hormone replacement therapy upon urinary prostaglandin E2 and prostaglandin F2 alpha levels in postmenopausal patients. A total number of 55 women were enrolled in this study and 15 premenopausal (PreM) healthy subjects constitute the control group. A total of 40 patients at least 12 months after their natural menopause were divided into two groups: 15 of them was not medicated hormone replacement therapy (which composed NRHRT group) while 25 of the rest, received conjugated estrogen (Premarin) 0.625 mg/day orally plus medroxyprogesterone acetate (Farlutal) 10 mg/day orally built up the RHRT group. PGE2 and PGF2 alpha levels were measured with PGE2 [125I] and PGF2 alpha [3H] RIA kits. Statistical significance was analyzed by Students t-test for impaired data. NRHRT and RHRT patients had had increased urinary PGE2 levels when compared with PreM (P < 0.001). HRT caused a significant decrease in PGE2 levels in menopausal women (P < 0.001). Urinary PGF2 alpha values of NRHRT and RHRT were significantly lower (P < 0.001) in comparison with PreM group. There was no difference in PGF2 alpha values between two postmenopausal groups. HRT given to postmenopausal patients might have a positive impact on prostaglandins and therefore on bone turnover in a series of various mechanisms.

Lipid profile in actinic keratosis and basal cell carcinoma.

Background The lipid content of the skin and its changes are important in the pathogenesis of many disorders affecting the skin, particularly actinic keratosis (AK) and basal cell carcinoma (BCC).

Urinary PGE2 and PGF2α Levels and Renal Functions in Preeclampsia

The role of prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) in the pathogenesis of hypertension and altered renal functions, which are the main symptoms of preeclampsia, has gained importance. Serum and urine samples of 59 women (24 preeclamptic pregnant (PEP), 20 normotensive pregnant (NTP) and 15 nonpregnant) were investigated by means of prostaglandin levels and urea, creatinine and creatinine clearance values. PEP patients, when compared with NTP patients, show a significant decrease in PGE2 and PGF2α levels (p < 0.01 and p < 0.05, respectively) accompanied by changes in some parameters of renal function such as serum urea, creatinine and creatinine clearance. Although disorders in prostaglandin levels may be responsible for some renal pathologic changes, renal functional and morphologic alterations may also result in abnormal prostaglandin activity.

Effects of Ibuprofen on the physiology and outcome of rabbit endotoxic shock

BackgroundDespite major developments in the management of septic shock, the mortality rate had progressively increased. Ibuprofen has been shown to have beneficial physiological effects when used as a treatment. However, there are conflicting results with respect to survival. This study aims to investigate the effect of ibuprofen on vital functions, various physiological parameters and survival during endotoxic shock in rabbits.MethodsTwenty-eight New Zealand rabbits were randomly separated into four groups. The first group received only saline, the second was given 2 mg/kg intravenous endotoxin at t0, the third received 30 mg/kg ibuprofen 30 minutes after endotoxin administration, whilst the fourth group received ibuprofen 30 minutes before the endotoxin. Respiratory and heart rate, mean arterial blood pressure and rectal temperature were recorded. Complete blood counts were performed and thromboxane B2 was measured every 30 minutes for the first two hours, and then hourly over the course of the experiment. Urine samples were collected at the same time points for the measurement of prostaglandin E2.ResultsIbuprofen was found to improve respiratory rate, heart rate, and arterial pressure. However, it did not improve the negative effects of endotoxin on body temperature, haematocrit values, white blood cell count, and thrombocyte number. Thromboxane B2 levels in group IV were significantly lower than in the other groups, and the increase started at a later timepoint. In ibuprofen-treated animals, Prostaglandin E2 levels stayed low for at least 90 minutes, but started to rise thereafter. While the average survival in Group II animals was 192.9 ± 46.9 minutes, those of groups III and IV were 339.1 ± 33.5 minutes (p < 0.05) and 383.0 ± 39.6 minutes (p = 0.01), respectively.ConclusionsIbuprofen appears to increase survival in endotoxic shock-induced animals. Therefore, it may be helpful for the prophylaxis and treatment of patients with, or who are likely to develop, septic shock.

Effects of ibuprofen on plasma endothelin levels and some vital parameters during endotoxin shock in rabbits

BACKGROUND There is evidence that septic shock results from breakdown in the balance between vasodilators such as prostacyclin, prostaglandin E(2), and nitric oxide, and the vasoconstrictors thromboxane A(2), serotonin, and endothelin. Increased plasma endothelin (ET) concentrations during septic shock were found. Inducing phospholipase A(2), ET causes release of arachidonic acid and production of prostaglandins. Ibuprofen is nonsteroidal anti-inflammatory drug inhibiting prostaglandin synthesis. There are no any information about the effects of ibuprofen on ET production in endotoxemia. In the present study we aimed to determine the effects of ibuprofen on plasma ET concentrations in an animal model of endotoxin shock. METHODS A total of 28 rabbits were randomly allocated into four groups. The first group only received saline and served as controls. The rest of the animals (groups 2, 3, and 4) were injected intravenously with endotoxin at a dose of 2 mg/kg. To the third group, ibuprofen at 30 mg/kg dosage was given, 30 min following endotoxin administration, whereas in the fourth group animals, ibuprofen was administered 30 min before endotoxin administration. Animals were monitored through the canulation of femoral arteries and venules under the complete anaesthesia. At 0, 30, 60, 90, 120, 180, and 240 min, arterial blood pressure, heart rate, and ET determinations were carried out. RESULTS Ibuprofen before the endotoxin administration was more effective in controlling the increase in heart rate. Ibuprofen was also effective in inhibiting the sudden reductions in blood pressure if administered before endotoxin. However, if administered after endotoxin injection, ibuprofen precipitated the reduction in blood pressure further. Ibuprofen reduced the ET production which was induced by the endotoxin administration. CONCLUSIONS Ibuprofen administration during endotoxin shock seems to decrease the elevated ET concentrations, and increase the blood pressure.