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Epidemiological studies suggest that n-3 polyunsaturated fatty acid (n-3 FA) deficiency is a risk factor for bipolar disorders (BDs). The aim of this study was to determine whether such a deficit does exist in patients with BD and to characterize the overall plasma fatty acid (FA) profile in these patients. Using gas chromatography/mass spectrometry, we measured fasting plasma levels of 15 FAs in 42 patients diagnosed with BD according to DSM-IV criteria and in 57 age- and gender-matched healthy controls. Plasma docosahexaenoic acid (DHA) levels were significantly decreased in bipolar patients (p < 0.001 versus healthy controls). Compared with controls, patients had higher plasma levels of all other FAs, including arachidonic acid (AA, p < 0.001), alpha-linolenic acid (ALA, p < 0.001), and eicosapentaenoic acid (EPA) (p < 0.001). Although in the present study we observed significant DHA deficits in the plasma of bipolar patients our findings do not support the therapeutic use of ALA and/or EPA supplementation. DHA may provide a basis for possible pharmacological intervention in psychiatric disorders at the level of second messengers linked to the phosphatidylinositol cycle. Finally, measurement of FA levels in plasma seems to be more reliable and reproducible than assays of erythrocyte FA content.

OBJECTIVES: We analyzed the relationships between sudden sensorineural hearing loss (SSNHL) and serum levels of fatty acids, total cholesterol, low-density lipoproteins (LDLs), and the antioxidant coenzyme Q10. METHODS: Forty-three patients with SSNHL and 43 healthy subjects were enrolled in the study. The main outcome measures were serum levels of fatty acids, coenzyme Q10, total cholesterol, and LDLs. RESULTS: On univariate logistic regression analysis, high levels of total cholesterol (p < 0.001), LDLs (p = 0.024), behenic acid (p < 0.001), docosahexaenoic acid (p < 0.001), linolenic acid (p = 0.017), and oleic acid (p < 0.001) and low levels of coenzyme Q10 (p < 0.001) and nervonic acid (p < 0.001) were associated with an elevated risk of SSNHL. On multivariate analysis, only hypercholesterolemia (p = 0.15) and low levels of coenzyme Q10 (p = 0.02) and nervonic acid (p = 0.005) were significantly associated with SSNHL. CONCLUSIONS: 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.

OBJECTIVES: We analyzed the relationships between sudden sensorineural hearing loss (SSNHL) and serum levels of fatty acids, total cholesterol, low-density lipoproteins (LDLs), and the antioxidant coenzyme Q10. METHODS: Forty-three patients with SSNHL and 43 healthy subjects were enrolled in the study. The main outcome measures were serum levels of fatty acids, coenzyme Q10, total cholesterol, and LDLs. RESULTS: On univariate logistic regression analysis, high levels of total cholesterol (p < 0.001), LDLs (p = 0.024), behenic acid (p < 0.001), docosahexaenoic acid (p < 0.001), linolenic acid (p = 0.017), and oleic acid (p < 0.001) and low levels of coenzyme Q10 (p < 0.001) and nervonic acid (p < 0.001) were associated with an elevated risk of SSNHL. On multivariate analysis, only hypercholesterolemia (p = 0.15) and low levels of coenzyme Q10 (p = 0.02) and nervonic acid (p = 0.005) were significantly associated with SSNHL. CONCLUSIONS: 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.

OBJECTIVES:: We investigated the association of idiopathic sudden sensorineural hearing loss (ISSNHL) with coenzyme Q (CoQ) and cardiovascular risk factors. STUDY DESIGN:: A prospective study. SETTING:: Hospital center. PATIENTS:: Thirty Italian patients with ISSNHL and 60 healthy Italian subjects. INTERVENTION:: Diagnostic. MAIN OUTCOME MEASURE:: Evaluation of serum CoQ levels and cardiovascular risk factors (total cholesterol, low-density lipoprotein [LDL], homocysteine [HCY]). The results were compared with variance analysis and Student's t test. Univariate and multivariate analysis were used to evaluate the association between ISSNHL and CoQ, total cholesterol, LDL, and HCY levels. RESULTS:: In our series, we found a significant association between ISSNHL and high total cholesterol (p < 0.05), high LDL (p = 0.021), and low CoQ (p < 0.05) levels. We did not find a significant association between ISSNHL and HCY levels. In the univariate analysis, low levels of CoQ, high levels of total cholesterol, and LDL were found to be significantly associated with ISSNHL. In the multivariate analysis, only high levels of total cholesterol and low levels of CoQ remained significantly associated with a high risk of sudden sensorineural hearing loss. CONCLUSION:: 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 toinvestigate the role of antioxidants, including CoQ, in ISSNHL.

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Experimental hyperoxia represents a suitable in vitro model to study some pathogenic mechanisms related to oxidative stress. Moreover, it allows the investigation of the molecular pathophysiology underlying oxygen therapy and oxygen toxicity. In this study, we adopted a modified experimental set up to accomplish a model of moderate hyperoxia (50% O2, 96 hours culture) in order to induce oxidative stress in the human leukemia cell line U-937. Spectrophotometric measurements of mitochondrial respiratory enzyme activities, NMR spectroscopy of culture media, determination of antioxidant enzyme activities, cell proliferation and differentiation assays were performed. Data showed that moderate hyperoxia in this myeloid cell line causes: i) an intriguing alteration of mitochondrial activities at the level of succinate dehydrogenase and succinate-cytochrome c reductase; ii) an induction of metabolic compensatory adaptations with a significant shift to glycolysis; iii) an induction of different antioxidant enzyme activities; iv) a significant cell growth inhibition; v) no significant apoptosis. This work permitted to better characterize the mitochondrial damage induced by hyperoxia. In particular, data showed a large increase of succinate cytochrome c reductase activity that could be a fundamental pathogenic mechanism at the basis of oxygen toxicity.

Coenzyme Q(10) (CoQ(10)), vitamin E, total cholesterol, HDL-cholesterol (HDLC) and triglycerides were measured in the plasma of 62 patients with kidney failure, 46 under hemodialysis treatment and 16 under conservative therapy, and 95 controls. The sum of LDL-cholesterol (LDL-C) and VLDL-cholesterol (VLDL-C) was also calculated for each patient. The ratio CoQ(10)/LDL-C+VLDL-C in both conservative therapy and hemodialysis populations was significantly lower (P<0.001) compared with normal controls and remained unchanged after the dialysis treatment. On the contrary the ratio vitamin E/LDL-C+VLDL-C was normal but decreased significantly (P<0.02) after each dialysis. Since coenzyme Q is the main inhibitor of the prooxidant action of vitamin E, it was hypothesized that its decrease in both the populations examined could make the lipoproteins of these patients more vulnerable to a peroxidative attack.

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Effect on neurotrophil chemiluminescence of middle molecular weight substances present in peritoneal dialysis fluid in patients with acute renal failure

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