The serum protein and lipid oxidation marker levels in Alzheimer's disease and effects of cholinesterase inhibitors and antipsychotic drugs therapy.

Oxidative stress plays an important role in the pathogenesis of Alzheimer's disease (AD). The aim of this study was to evaluate the serum oxidation marker levels in patients with AD. Both untreated patients (n: 15) and patients who received treatment (n: 62) had higher Malondialdehyde (p<0.01 and p<0.001), Oxidized LDL (ox-LDL; p<0.0001 and p<0.0001), F(2)-isoprostane (p<0.0001 and p<0.001), and Nitric oxide (NOx; p<0.0001 and p<0.0001) levels compared with those of age-matched controls (n: 15). Protein Carbonyl and Asymmetrical Dimethyl-L-Arginine levels in Alzheimer patients were not found to be different from the controls. Short-term cholinesterase inhibitor (ChEIs) therapy (7, 5 +/-1, 5 months, n: 12) resulted in a reduction in ox-LDL and NOx levels (p<0.05 and p<0.01) from baseline. Long-term ChEI- therapy group (50, 4+/- 30, 5 months, n: 33) has higher ox-LDL, NOx and F(2)-isoprostane levels than short-term treated group (p<0.01, p<0.001 and p<0.05, respectively). Ox-LDL levels were also found to be lower in ChEI patients who were given antipsychotic treatment (n: 15) than in the group who were ChEIs-alone treatment group (p<0.0001). MMSE scores showed negative correlation with both NOx (p<0.05) and ox-LDL (p<0.05) levels. There was positive correlation between NOx and both MDA (p<0.05) and ox-LDL (p<0.05), and between F(2)-isoprostane and 3-NT (p<0.05). In conclusion, our results suggest that serum NOx-induced lipid oxidation levels were increased in AD and use of antipsychotic drugs may cause lower ox-LDL levels in patients having combination therapy with ChEi's. However, it is required further studies for the determination of clinical importance of these markers.

The effects of hormone replacement therapy on lipid peroxidation and antioxidant status.

OBJECTIVE: A number of studies have consistently shown a lower cardiovascular risk in women who received postmenopausal hormone replacement therapy (HRT). The aim of our study was to examine the effects of HRT on lipid peroxidation and antioxidant status, which were likely to be involved in the pathophysiology of atherosclerosis. METHODS: We measured erythrocyte and plasma thiobarbituric acid reactive substances (TBARS) levels as expression of lipid peroxidation-end product malondialdehyde, and also erythrocyte reduced glutathione (GSH) level and glutathione peroxidase (GSH-Px) activity as indicators of the antioxidant status of the 35 postmenopausal women with HRT (mean age: 51.81 +/- 4.57 yr; body mass index (BMI): 26.56 +/- 3.78 kg/m(2)) and 35 postmenopausal women without HRT (mean age: 47.50 +/- 3.64; BMI: 27.42 +/-3.43 kg/m2). RESULTS: In the group with HRT, erythrocyte and plasma TBARS levels were significantly lower than in the group without HRT (P < 0.003 and P < 0.001, respectively). Erythrocyte GSH level and GSH-Px activity was found to be increased significantly in the group with HRT in comparison with the group without HRT (P < 0.001 and P < 0.001, respectively). There was not any correlation between the erythrocyte and plasma TBARS and erythrocyte GSH levels and GSH-Px activity with duration of HRT (mean 3.5+/-1.3 yr). CONCLUSION: Our results show that HRT is beneficial in the protection against oxidative damage and can prevent atherosclerotic complications.