Ratio Of Serum Vitamin Research Articles

Concentrations of Antioxidant Vitamins in Maternal and Cord Serum and Their Effect on Birth Outcomes

Emerging evidence indicates that maternal oxidative stress during pregnancy could impair fetal growth and that antioxidant vitamins (e.g. vitamins A, E and C) have a significant role in maintaining physiological processes of pregnancy and growth. To determine the concentrations of vitamins A, E, and C in pair-matched maternal and cord serum samples of neonate, and thus to investigate the relationship between maternal serum levels of these vitamins at delivery and birth outcomes. A total of 143 mother-neonate pairs were recruited into the cross-sectional descriptive study. Demographic information was investigated by questionnaire. After delivery, both cord and maternal blood were collected for quantification of serum levels of vitamins A, E and C by HPLC. Maternal serum levels of vitamins A and E were significantly higher than those in cord serum. In contrast, vitamin C level in cord serum was significantly higher than that in maternal serum. Further, we found that maternal vitamin A status was significantly correlated to both birth weight (r=0.19, p=0.0419) and birth height (r=0.21, p=0.0311), and these were manifested by these findings: (i) per 250.2 g reduction in birth weight concomitant with 1 micromol/L increase in maternal serum vitamin A level (p<0.01; 95% CI: 56.9-451.5); and (ii) per 1% increase in the ratio of serum vitamin A level of neonate to mother concomitant with 0.8 cm increase in birth height (p=0.049; 95% CI: 0.004-1.639). Maternal vitamin A, but not vitamins E and C, during pregnancy had a significant effect on birth outcomes. Further studies are necessary to investigate the role of these antioxidant vitamins in fetal growth at various gestation stages.

Oxidation of serum low-density lipoprotein (LDL) and antioxidant status in young and elderly humans

The incidence of atherosclerosis increases with age, as do various indices of free-radical mediated damage, e.g., lipid peroxidation. Because lipid peroxidation plays a prominent role in lipoprotein oxidation, likely a prelude to atherosclerosis, we compared the susceptibility of lipoproteins to oxidation in young (19–30 years) and elderly (59–86 years) groups. Although we found no significant differences in serum malondialdehyde (MDA) or oxidized LDL antibodies (OLAB) between young and elderly lipoproteins, MDA was directly related to OLAB regardless of age ( r = 0.322, p = 0.005) and there was a trend for lower OLAB levels (30.5%, p = 0.079) in the elderly compared to the young population. Overall, serum antioxidant status was either similar or greater in the elderly group compared to the young group, likely reflecting antioxidant supplementation by the elderly group. OLAB was inversely related to Vitamin C ( r = −0.310, p = 0.008) and Vitamin E intake ( r = −0.277, p = 0.018) from foods and supplements. Serum levels of Vitamin C and Vitamin E were significantly higher (18.5%, p = 0.021 and 58.1 %, p < 0.001, respectively) in the elderly group compared to the young group and the ratio of Vitamin E to Vitamin C was significantly higher (30.4%, p = 0.042) in the serum of the elderly group. Oxidation of serum LDL and antioxidant status were not affected by age; however, the ratio of serum Vitamin E to Vitamin C was higher in the elderly group which may affect Vitamin E recycling.

Hypocholesterolemic Effect of Pravastatin is Associated with Increased Content of Antioxidant Vitamin-E in Cholesterol Fractions

Metabolic studies support the findings that antioxidants inhibit atherosclerosis. Treatment with vitamin E reduced both the susceptibility of low density lipoprotein cholesterol (LDL-C) to in vivo lipid peroxidation and atherosclerosis and smooth muscle proliferation. Thus the aim of present study was to examine metabolic consequences of reduced plasma LDL-C during hypolipidemic therapy and the distribution of antioxidant vitamin E. A group of 10 patients (4 men, 6 women, age 35-65y) with familial hypercholesterolaemia was treated using pravastatin (Lipostat Bristol Myers Squibb, 40 mg daily at 6:00 PM). Blood samples were examined before treatment, after 4 and 8 weeks of therapy. After ultracentrifugation, samples were analyzed for lipoprotein fractions and the content of vitamin E and cholesterol. Pravastatin reduced both total cholesterol (9.85 +/- 0.74 vs. 6.81 +/- 0.51 mmol/1; p < 0.01), LDL-C (6.42 +/- 0.45 vs. 4.51 +/- 0.45 mmol/l; p < 0.01), light LDL1-C (4.56 +/- 0.50 vs. 3.11 +/- 0.34 mmol/l; p < 0.05) and dense LDL2-C (1.86 +/- 0.27 vs. 1.42 +/- 0.17 mmol/l; ns). Serum vitamin E was reduced during hypolipidemic therapy in the fraction of total, LDL1, LDL2, and VLDL-cholesterol. However, the ratio of serum vitamin E/total serum cholesterol (4.57 +/- 0.32 vs. 5.12 +/- 0.37 mmol/l/mmol/l; p < 0.05) and ratio of LDL2-C vitamin E/LDL2-C (3.92 +/- 0.07 vs. 4.64 +/- 0.37 mmol/l/mmol/l; p = 0.08) increased in comparison to pre-treatment values. We conclude that pravastatin therapy may possess anti-atherogenic properties which involve not only its hypocholesterolemic effect, but also its favorable effects on the distribution of LDL subclasses and the content of antioxidant vitamin E in atherogenic lipoproteins.

STUDY OF VITAMIN A SUPPLEMENTATION IN CAPTIVE NORTHERN FUR SEALS (CALLORHINUS URSINUS) AND ITS EFFECT ON SERUM VITAMIN E

AbstractTwo experiments were conducted to determine the effect of vitamin A supplementation on serum vitamin E in adult female northern fur seals (Callorhinus ursinus). In the first experiment five animals received, in addition to their routine dietary multivitamin supplement, a high‐level vitamin A supplement (53 μmol retinyl palmitate/d) for 30 d. Five seals consuming their routine dietary supplement served as controls. Serum vitamin E decreased significantly in animals receiving high‐level vitamin A supplements. At the end of 30 d serum vitamin E averaged 18.6 μg/mL in the control animals and 13.4 μg/mL in the animals receiving the high‐Ieve1 vitamin A supplement. In experiment 2 ten animals received the high level vitamin A supplement for 60 d. After 30 d, serum vitamin E levels were reduced, but by 60 d had returned to baseline levels. However, the ratio of serum vitamin E to phospholipid, another index of vitamin E status, remained decreased. Although the exact mechanism of interaction is unknown, this study shows that when providing vitamin supplements for captive pinnipeds, vitamin interactions must be considered. The vitamin A supplementation currently used by some institutions seems unnecessary and may have detrimental effects on vitamin E status.

Genetic hemochromatosis and Wilson'S disease: Role for oxidant stress?

Hereditary haemochromatosis is characterised by iron overload that may lead to tissue damage. Free iron is a potent promoter of hydroxyl radical formation that can cause increased lipid peroxidation and depletion of chain-breaking antioxidants. We have therefore assessed lipid peroxidation and antioxidant status in 15 subjects with hereditary haemochromatosis and age/sex matched controls. Subjects with haemochromatosis had increased serum iron (24.8 (19.1-30.5) vs. 17.8 (16.1-19.5) μmol/L, P = 0.021) and % saturation (51.8 (42.0-61.6) vs. 38.1 (32.8-44.0), P = 0.025). Thiobarbituric acid reactive substances (TBARS), a marker of lipid peroxidation, were increased in haemochromatosis (0.59 (0.48-0.70) vs. 0.46 (0.21-0.71) μmol/l, P = 0.045), and there were decreased levels of the chain-breaking antioxidants alpha-tocopherol (5.91 (5.17-6.60) vs. 7.24 (6.49-7.80) μmol/mmol cholesterol, P = 0.001), ascorbate (51.3 (33.7-69.0) vs. 89.1 (65.3-112.9), P = 0.013), and retinol (1.78 (1.46-2.10) vs. 2.46 (2.22-2.70) μmol/l, P - 0.001). Patients with hereditary haemochromatosis have reduced levels of antioxidant vitamins, and nutritional antioxidant supplementation may represent a novel approach to preventing tissue damage. However, the use of vitamin C may be deleterious in this setting as ascorbate can have prooxidant effects in the presence of iron overload. The RRR-alpha-tocopherol (vitamin E) content in plasma from 46 patients with liver diseases and 23 healthy controls was determined by high performance liquid chromatography and electrochemical detection. Patients were divided into three groups: alcoholic liver diseases (n = 17; group A), hemochromatosis (n 17;group B) and Wilson's disease (n 12;group C). Lipidstandardized alpha-tocopherol levels were determined to neutralize differences due to hyperlipemia. The ratio of serum vitamin E to serum lipids (cholesterol, triglycerides, phospholipids) was highest in healthy controls and in patients in group A with cirrhosis and normal transaminases and bilirubin. Patients in group A with acute or chronic ethanol intoxication and high bilirubin levels had a 37% lower lipid-standardized vitamin E level than controls. Patients in group B with hemochromatosis, showing high serum iron (&gt;180 μg/dl), a low free iron binding capacity (&lt;8 μmol/l) and high ferritin-levels (&gt;450 μg/l), had a 34% lower vitamin E/lipid ratio than healthy controls. No significant lowering of the vitamin E/lipid ratio was observed in the other patients in group B. A significant decrease (37%) in the vitamin E/lipid ratio was only detectable in patients with Wilson's disease (group C) showing high free serum copper (&gt;10 μg/dl). The data support a role for free radicals in the pathogenesis of active liver diseases. © Journal of Hepatology.

Low vitamin E content in plasma of patients with alcoholic liver disease, hemochromatosis and wilson's disease

The RRR-alpha-tocopherol (vitamin E) content in plasma from 46 patients with liver diseases and 23 healthy controls was determined by high performance liquid chromatography and electrochemical detection. Patients were divided into three groups: alcoholic liver diseases (n = 17; group A), hemochromatosis (n = 17; group B) and Wilson's disease (n = 12; group C). Lipid-standardized alpha-tocopherol levels were determined to neutralize differences due to hyperlipemia. The ratio of serum vitamin E to serum lipids (cholesterol, triglycerides, phospholipids) was highest in healthy controls and in patients in group A with cirrhosis and normal transaminases and bilirubin. Patients in group A with acute or chronic ethanol intoxication and high bilirubin levels had a 37% lower lipid-standardized vitamin E level than controls. Patients in group B with hemochromatosis, showing high serum iron (> 180 micrograms/dl), a low free iron binding capacity (< 8 mumol/l) and high ferritin-levels (< 450 micrograms/l), had a 34% lower vitamin E/lipid ratio than healthy controls. No significant lowering of the vitamin E/lipid ratio was observed in the other patients in group B. A significant decrease (37%) in the vitamin E/lipid ratio was only detectable in patients with Wilson's disease (group C) showing high free serum copper (> 10 micrograms/dl). The data support a role for free radicals in the pathogenesis of active liver diseases.

Comparison of Total Serum Lipids Measured by Two Methods

Summaryto accurately assess vitamin E status, the ratio of serum vitamin E to total serum lipids is required. We compared two methods of measuring total serum lipids: (a) the calculated sum of measured cholesterol, triglycerides, and phospholipids, and (b) the colorimetric method. Over the entire range of total lipid concentrations (151–1,728 mg/dl), there was an excellent correlation between methods (r = 0.930; p &lt; 0.001). No significant differences between measurements by these methods were found over the entire range and between 0 and 1,000 mg/dl; however, between 1,000 and 1,728 mg/dl, the measured total lipid concentration was higher (p = 0.023) than the added total lipid measurements. Despite this discrepancy, the methods appear comparable for clinical use in assessing vitamin E/total lipid status; the measured total lipids would be the preferred method because of the low cost and ease of performance of the test.

Comparison of Total Serum Lipids Measured by Two Methods

To accurately assess vitamin E status, the ratio of serum vitamin E to total serum lipids is required. We compared two methods of measuring total serum lipids: (a) the calculated sum of measured cholesterol, triglycerides, and phospholipids, and (b) the colorimetric method. Over the entire range of total lipid concentrations (151-1,728 mg/dl), there was an excellent correlation between methods (r = 0.930; p less than 0.001). No significant differences between measurements by these methods were found over the entire range and between 0 and 1,000 mg/dl; however, between 1,000 and 1,728 mg/dl, the measured total lipid concentration was higher (p = 0.023) than the added total lipid measurements. Despite this discrepancy, the methods appear comparable for clinical use in assessing vitamin E/total lipid status; the measured total lipids would be the preferred method because of the low cost and ease of performance of the test.

Intestinal Malabsorption of Vitamin E in Primary Biliary Cirrhosis

We studied intestinal absorption of vitamin E in 26 adults with primary biliary cirrhosis (PBC) and 6 control subjects. Seven (27%) PBC patients were vitamin E-deficient based on the ratio of serum vitamin E to serum total lipid concentrations. An oral vitamin E tolerance test was performed in all patients and control subjects using a loading dose of 2000 IU alpha-tocopheryl acetate with measurement of serial serum vitamin E concentrations over 24 h. Vitamin E absorption was expressed as the maximal rise in serum vitamin E above baseline, the area under the oral tolerance test curve, and these two values divided by the fasting total serum lipid concentration. Absorption of vitamin E was significantly impaired in all PBC patients vs. control subjects (p less than 0.01), in vitamin E-deficient vs. vitamin E-sufficient PBC patients (p less than 0.05 to p less than 0.01), and in PBC patients with serum vitamin E levels below 10 micrograms/ml vs. those with serum vitamin E levels above 10 micrograms/ml (p less than 0.01). Vitamin E absorption was inversely related to stage of PBC, serum cholylglycine, total bilirubin, cholesterol, alkaline phosphatase, aspartate aminotransferase, and prothrombin time. Patients with serum vitamin E below 10 micrograms/ml, serum total bilirubin above 3 mg/dl, serum cholylglycine above 600 micrograms/dl, or serum alkaline phosphatase above 1000 IU/L had severe malabsorption of vitamin E and would be at high risk for the development of vitamin E deficiency. Therefore, vitamin E supplementation should be considered not only in patients in whom overt vitamin E deficiency is present, but also in PBC patients meeting these criteria.

Vitamin E deficiency and its clinical significance in adults with primary biliary cirrhosis and other forms of chronic liver disease

The vitamin E status of 146 adults with chronic liver disease was assessed by estimating both their serum vitamin E concentration and the ratio of serum vitamin E to serum cholesterol concentration. Low levels of vitamin E occurred most frequently in patients with primary biliary cirrhosis and other forms of chronic cholestatic liver disease. When a serum vitamin E concentration of 12.3 mumol/l (mean-2 SD of a control population) was taken as the lower limit of normal, 44% of patients with primary biliary cirrhosis and 32% with other chronic cholestatic liver disease had a reduced concentration, indicating a biochemical deficiency of vitamin E. If a vitamin E/total cholesterol ratio of 2.35 mumol/mmol was taken as the lower limit of normal, then 64% and 43% of patients with primary biliary cirrhosis and other chronic cholestatic liver disease, respectively, had a biochemical deficiency of vitamin E. Of the patients with chronic cholestasis and a serum bilirubin concentration greater than 100 mumol/l, 91% had a reduced vitamin E/cholesterol ratio. Twelve patients with primary biliary cirrhosis and severe vitamin E deficiency (serum vitamin E less than 5.0 mumol/l and a vitamin E/cholesterol ratio less than 1.0 mumol/mmol) underwent extensive neurological investigation. Five had a mild mixed sensorimotor peripheral neuropathy, which was not, however, typical of the neurological syndrome associated with vitamin E deficiency. In patients with severe biochemical deficiency of vitamin E (less than 5 mumol/l and less than 1 mumol/mmol total cholesterol), administration of large oral doses of vitamin E only increased serum concentrations to within the normal range in one patient; in the others even weekly parenteral administration over a 3-month period did not correct deficiency. In patients with less severe biochemical deficiency, the serum vitamin E concentration and vitamin E/total cholesterol ratio were restored to normal by oral or intramuscular supplements of the vitamin.

Vitamin E deficiency in adults with chronic liver disease

In order to determine the frequency of vitamin E deficiency in adults with chronic liver disease, we measured serum vitamin E concentrations and calculated the ratio of serum vitamin E to total serum lipids (E/lipids) in forty-two patients with primary biliary cirrhosis (PBC) (Group A), fifteen patients with other forms of chronic liver disease (Group B), and twenty-five healthy adult control subjects (Group C). Although the mean serum vitamin E concentration did not differ significantly among the three groups, the ratio of serum vitamin E/lipids was significantly lower in Group A than Groups B and C. Vitamin E deficiency, as defined by the ratio of serum vitamin E/lipids below 0.8 mg/gm, was present in seven (17%) Group A and one (7%) Group B patients. Serum cholylglycine, sulfated lithocholate conjugates, and bilirubin were significantly higher and the mean duration of symptomatic primary biliary cirrhosis was significantly longer (6.6 vs 2.3 years) in the vitamin E-deficient compared to the vitamin E-sufficient Group A patients. Our study demonstrates that vitamin E deficiency may occur in adults with severe, prolonged cholestatic liver disease.