RESUMEN
Background: The protective effect of bilirubin relates to the antioxidant property of bilirubin, which prevents lipid oxidation, especially low-density lipoprotein (LDL), and inhibits free radical-induced dam-ages. Lower serum bilirubin level has been proven to be associated with endothelium and microvascular malfunction. The aim of the present study was to assess the association between serum bilirubin levels and coronary artery disease in comparison with controls without coronary artery disease.Methods: A cross-sectional study was conducted for a period of a one year in our medical college hospital. Patients with evidence of coronary artery disease for not more than 10 years of duration confirmed by ECG, ECHO and other previous case records were taken as cases. Controls were selected matched with age, gender and other co-morbid conditions. Total of 200 subjects were included in the study with 100 cases and 100 controls. General and systemic examination was conducted on all study subjects including laboratory investigations like complete blood count, renal function test, lipid profile, viral markers such as HBsAG, HCVIgM and liver function test which includes total bilirubin, direct and indirect, liver enzymes, albumin and globulin levels. A 12 lead ECG and a transthoracic echocardiogram was performed for all patients.Results: The various liver function test parameters were compared between the cases and controls it was found that the serum bilirubin levels which includes total bilirubin, direct bilirubin and indirect bilirubin was found to be lower among the case group compared to the control group and this difference was found to be statistically significant (p <0.05). A perfect linear correlation between the ejection fraction and serum bilirubin levels, as the ejection fraction decreases the serum bilirubin levels was also decreasing.Conclusions: This study showed a significant association between the reduced serum bilirubin levels and the occurrence of CAD; therefore, bilirubin level can serve as a predictive factor, together with other influential factors for identifying a person at risk of developing coronary artery disease.
RESUMEN
A study on the effect of retinol in vitro on the hemolysis of vitamin Ε deficient rat red blood cells showed that retinol enhanced the lysis of the Ε deficient cells as compared to the lysis of normal cells. The lipid peroxidation present during hydrogen peroxide induced lysis of Ε deficient cells was however markedly inhibited in the presence of retinol without affecting the rate of lysis. In an actively peroxidising system of non-enzymatic lipid peroxidation of rat liver or brain homogenates and of brain lysosomes incubated with human erythrocytes, no lysis was obtained; incorporation of retinol in such systems resulted in lysis but no peroxidation. Hydrogen peroxide generating substances almost completely inhibited the lysis of normal human erythrocytes by retinol, but linoleic acid hydroperoxide and auto-oxidised liver or brain homogenates and ox-brain liposomes increased the lysis. It is concluded that vitamin Ε deficient erythrocyte hemolysis may be augmented by retinol, an anti-oxidant, having a lytic function without the peroxidation of stromal lipids.
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An aldolase was partially purified from fermenter grown Mycobacterium tuberculosis H37Rv cells. The aldolase has a molecular weight of 150,000, possesses a tetrameric structure and cleaves both fructose diphosphate and fructose- 1-phosphate, the former being cleaved 17 times faster. The enzyme was inactivated by treatment with NaBH4 in the presence of fructose diphosphate or dihydroxyacetone, phosphate suggesting Schiff base formation during its catalytic function. Thiol reagents, EDTA and metal ions had no apparent effect on the aldolase activity. These results show that aldolase is of Class I type. However, this enzyme, unlike the mammalian Class I aldolase, was unaffected by carboxypeptidase A. Nethylmaleiniide and dithionitrobenzoic acid.
RESUMEN
The results presented in this paper show that lysis of human erythrocytes by linoleic acid is not caused by peroxidation of the fatty acid. Peroxidase, superoxide dismutase and scavengers of Ο · and OH had no effect on the lysis while catalase showed only marginal inhibition suggesting that Ο , OH , O and H2O2 do not play any direct role in hemolysis by linoleic acid. Generators of H2O2 inhibited the lysis completely and methemoglobin cells were more resistant to hemolysis by linoleic acid. The fatty acid did neither bind to nor fomed complex with red cell ghosts. Membrane oxidation of sulphydryl groups was also not involved in the lysis. β-Carotene, retinol and bile salts enhanced the lysis, while, cholesterol but not cholesterol acetate, inhibited it. Taurocholate-pretreated cells were more susceptible to linoleic acid lysis. These observations suggested-that lysis by linoleic acid may be due to its detergent property.
RESUMEN
An enzyme catalysing the hydrolysis of a-tocopheryl acetate was characterised in chicken liver. The enzyme was localised in the microsomes, had an optimum pH 8·6 and a Km value of 0·5 mM. The enzyme did not hydrolyse retinyl acetate, cholesteryl acetate and ethyl acetate, thus indicating a high degree of specificity. a-Tocopheryl acetate hydrolase required bile salts as a specific cofactor. The results suggested a role for this enzyme in the absorption of vitamin E.