Inhibitors of HMG-CoA reductase are new safe and effective cholesterol-lowering agents. Elevation of alanine-amino transferase (ALT) and aspartate-amino transferase (AST) has been described in a few cases and a myopathy with elevation of creatinine kinase (CK) has been reported rarely. The inhibition of HMG-CoA reductase affects also the biosynthesis of ubiquinone (CoQ10). We studied two groups of five healthy volunteers treated with 20 mg/day of pravastatin (Squibb, Italy) or simvastatin (MSD) for a month. Then we treated 30 hypercholesterolemic patients in a double-blind controlled study with pravastatin, simvastatin (20 mg/day), or placebo for 3 months. At the beginning, and 3 months thereafter we measured plasma total cholesterol, CoQ10, ALT, AST, CK, and other parameters (urea, creatinine, uric acid, total bilirubin, gamma GT, total protein). Significant changes in the healthy volunteer group were detected for total cholesterol and CoQ10 levels, which underwent about a 40% reduction after the treatment. The same extent of reduction, compared with placebo was measured in hypercholesterolemic patients treated with pravastatin or simvastatin. Our data show that the treatment with HMG-CoA reductase inhibitors lowers both total cholesterol and CoQ10 plasma levels in normal volunteers and in hypercholesterolemic patients. CoQ10 is essential for the production of energy and also has antioxidative properties. A diminution of CoQ10 availability may be the cause of membrane alteration with consequent cellular damage.
Chronic hypoxia (CH) is believed to induce myocardial protection, but this is in contrast with clinical evidence. Here, we test the hypothesis that repeated brief reoxygenation episodes during prolonged CH improve myocardial tolerance to hypoxia-induced dysfunction. Male 5-week-old Sprague-Dawley rats (n = 7–9/group) were exposed for 2 weeks to CH (F1O2 = 0.10), intermittent hypoxia (IH, same as CH, but 1 hr/day exposure to room air), or normoxia (N, F1O2 = 0.21). Hearts were isolated, Langendorff perfused for 30 min with hypoxic medium (Krebs-Henseleit, PO2 = 67 mmHg), and exposed to hyperoxia (PO2 = 670 mmHg). CH hearts displayed higher end-diastolic pressure, lower rate-pressure product, and higher vascular resistance than IH. During hypoxic perfusion, anaerobic mechanisms recruitment was similar in CH and IH hearts, but less than in N. Thus, despite differing only for 1 hr daily exposure to room air, CH and IH induced different responses in animal homeostasis, markers of oxidative stress, and myocardial tolerance to reoxygenation. We conclude that the protection in animals exposed to CH appears conferred by the hypoxic preconditioning due to the reoxygenation rather than by hypoxia per se.
This is the first report of low serum levels of nervonic acid as an independent risk factor for SSNHL. Considering that hypercholesterolemia, high serum levels of LDL, and low serum levels of the antioxidant coenzyme Q10 were associated with SSNHL as well, we hypothesize that saturated fatty acids may play a role in determining the dysmetabolic state in a subset of SSNHL patients. Together, these findings suggest that not only total cholesterol and LDL levels, but also fatty acid determination, may help identify SSNHL patients with cardiovascular risk factors.
The studies regarding the role of cardiovascular risk factors in ISSNHL are not conclusive. This is the first report regarding the association of ISSNHL and low serum levels of the antioxidant CoQ. Further studies are needed to investigate the role of antioxidants, including CoQ, in ISSNHL.
SUMMARY Neutrophil chemiluminescence was determined in patients with active rheumatoid arthritis. Twelve patients were randomly assigned either to a diet high in polyunsaturated fatty acids supplemented with eicosapentaenoic and docosahexaenoic acids or to a diet high in saturated fatty acids. A correlation with clinical and laboratory parameters is also reported. No statistical difference was observed in neutrophil chemiluminescence and in clinical parameters in the group of patients treated with a diet high in saturated fatty acids. Fish oil ingestion resulted in subjective alleviation of active rheumatoid arthritis and reduction of neutrophil chemiluminescence. This study corroborates the hypothesis of an anti-inflammatory role for polyunsaturated fatty acids in patients with chronic inflammatory diseases.Dietary composition has been shown to influence the immune response both in animals and in humans.' Therefore dietary manipulations may form the basis for a nutritional approach to treating autoimmune disorders.The regulatory effect of dietary lipid composition on many biological processes is well known.24 The ratio polyunsaturated:saturated fatty acids (P:S ratio) and the n-3 fatty acid amount are the important factors. Whereas the P:S ratio regulates the concentration of plasma cholesterol,S the n-3 fatty acids (eicosapentaenoate 20:5, docosahexaenoate 22:6) are mainly involved in the regulation of arachidonate metabolism.6The main source of eicosapentaenoic acid and docosahexaenoic acid is fish derived oil and an adequate dietary content seems to be 2-5 g/day.The relation between dietary factors and rheumatoid arthritis is becoming more evident.7 8 Furthermore, patients with rheumatoid arthritis (RA) show a notable increase of arachidonate metabolism via lipoxygenase, leading to leucotrienes B4 or D4.9Recently, Lee et al presented evidence for an inhibitory effect on polymorphonuclear activity of a diet rich in n-3 fatty acids.10
In a group of 48 chronic hemodialysis patients, serum levels of coenzyme Q10 (CoQ) have been measured and appeared abnormally low in 62% of cases. Figures were positively correlated to those of serum vitamin E (vit E), although the latter were within a normal range. The chronic hemodialysis (CHD) patients with normal serum values of CoQ exhibited higher blood triglycerides. Pathologically low levels of serum vit E were found only in uremic subjects on conservative regimen with dietary restrictions and low compliance to protein-caloric intake. The reduced CoQ levels may contribute to the defective serum antioxidant activity and the increased peroxidative damage in uremic patients on CHD.
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