Lipase-catalyzed syntheses of monoglycerides by hydrolysis of soybean oil in AOT/isooctane reversed micelles.
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Biomedical subjects
Publications and source records attributed to S G Cao.
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The effect of administration of exogenous thyroxine on mitochondrial phosphatidylglycerol content and biosynthesis was investigated in rat heart ventricles. Rats were treated for 5 consecutive days with thyroxine (250 mg/kg body weight) and on the sixth day after an overnight fast the mass of ventricular mitochondrial phosphatidylglycerol and cardiolipin content were determined. Saline-treated animals served as controls. Thyroxine treatment did not affect body weight but increased heart weight 30% compared with controls. In addition, the ratio of heart weight/body weight (x 1000) was increased from 0.69 in controls to 0.89 in thyroxine-treated rats consistent with this model. Thyroxine-treatment resulted in a 34% increase (P < 0.05) in phosphatidylglycerol and a 23% increase (P < 0.05) in cardiolipin content in ventricular mitochondrial fractions compared with controls. The mechanism for the increase in ventricular mitochondrial phosphatidylglycerol was investigated. Phosphatidic acid:cytidine-5'-triphosphate-1,2-diacylglycerol cytidylyltransferase and phosphatidylglycerolphosphate phosphatase activities were unaltered in the ventricular mitochondria of thyroxine-treated rats. In contrast, phosphatidylglycerolphosphate synthase activity was increased 3.5-fold (P < 0.05) in these mitochondrial fractions compared with controls. As a control for the effectiveness of thyroxine on mitochondria, cardiolipin synthase activity was determined. A 2.8-fold increase (P < 0.05) in cardiolipin synthase activity was observed in ventricular mitochondrial fractions of thyroxine-treated rats compared with controls. We postulate that thyroxine-treatment of rats produces an increase in the pool size of ventricular mitochondrial phosphatidylglycerol and that the mechanism is an increase in phosphatidylglycerolphosphate synthase activity.
De novo biosynthesis of phosphatidylglycerol and cardiolipin in the isolated intact rat heart was shown to occur from newly synthesized phosphatidic acid via the formation of cytidine-5'-diphosphate-1,2-diacylglycerol (Hatch, G.M. (1994) Biochem. J. 297, 201-208). The biosynthesis of new cardiolipin was investigated in isolated rat hearts perfused with exogenous phosphatidylglycerol. Phosphatidylglycerol was rapidly (within 5 min) incorporated into the heart when hearts were perfused with either phosphatidyl-[14C]glycerol or NBD-phosphatidylglycerol. In hearts perfused with phosphatidyl-[14C]glycerol for up to 30 min the amount of radioactivity observed in phosphatidylglycerol was maximum by 5 min of perfusion and remained constant throughout the perfusion period. In the presence of 1-50 microM phosphatidylglycerol, the amount of radioactive phosphatidylglycerol incorporated into the heart was not affected. There was a time-dependent accumulation of radioactivity incorporated into cardiolipin. In addition, radioactivity was incorporated with time into lysophosphatidylglycerol. No significant amount of radioactivity was associated with other phospholipids involved in the biosynthesis of cardiolipin, including phosphatidic acid and cytidine-5'-diphosphate-1,2-diacylglycerol, precursors of cardiolipin biosynthesis via the CDP-DG pathway. We postulate that cardiac cardiolipin may be synthesized from exogenous phosphatidylglycerol independent of phosphatidylglycerol synthesized within the heart.
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Biosynthesis of phosphatidylglycerol (PG) and cardiolipin (CL) were investigated in perfused hearts of diabetic rats 4 days or 28 days after streptozotocin injection. Sham-injected and insulin-treated diabetic rats were used as controls. In addition, another group of rats fasted for 54 h was examined. Isolated rat hearts from these groups were perfused for 30 min with [32P]P(i), and the radioactivity incorporated into PG and CL and their pool sizes were determined in heart ventricles. There was no difference in the amount of radioactivity incorporated into CL, PG or other phospholipids between all groups. In addition, the pool sizes of CL and other phospholipids were unaltered. However, a striking decrease in the pool size of PG was observed in both diabetic and fasted rats compared to sham- and insulin-treated controls at 4 days after streptozotocin injection. The decrease in PG mass in diabetic rats was rapid (within 24-48 h) and was localized to cardiac membranes. Diabetes did not affect the activity of the enzymes of PG and CL biosynthesis in the mitochondrial fraction, or phospholipase A activity in subcellular fractions prepared from rat heart homogenates. In addition, pulse-chase experiments confirmed that diabetes did not affect the rate of new PG or CL biosynthesis. Since radioactivity associated with PG was unaltered in continuous-pulse perfusion experiments, a calculated 1.8-fold increase in the specific radioactivity of cardiac PG was observed in the hearts of acute diabetic rats compared with controls. Since the radioactivity incorporated into PG and CL, and the rate of CL biosynthesis, were unaltered in diabetic-rat hearts compared with controls, new CL was probably synthesized from newly synthesized PG. We postulate the existence of distinct pools of PG in the heart, and that the pool of newly synthesized PG used for CL biosynthesis does not appear to mix immediately with the pre-existing pool of PG in the isolated intact rat heart.
In this paper, we used Ca-alginate gel beads coated with polyetheneimine and glutaraldehyde to adsorb Expansum penicillium lipase. The immobilized lipase catalyzed esterification of 1-dodecanol with dodecanoic acid in benzene. The results show that when the concentration of Ca-alginate, polyetheneimine (PEI) and glutaraldehyde is 1%, 6% and 1%, respectively, the activity of the immobilized lipase and the amount of adsorbed protein are the highest. The immobilized lipase is better than the SDS-immobilized lipase. The activity of the immobilized lipase connected by glutaraldehyde is higher than the activity of that without glutaraldehyde. The initial rate of the immobilized lipase and lyophilized lipase powder is 5.9 x 10(2) nmol/min.mgpr and 2.8 x 10(1) nmol/min.mgpr, respectively. After the immobilized lipase catalyzed the esterification reaction at 37 degrees C for about 12 hours, 93.3% of 1-dodecanol was converted to ester, but for lyophilized lipase powder, only 17.5% converted. Based on all above results, we have presumed and explained the structure of this kind of immobilized lipase.
Phosphatidylglycerolphosphate (PGP) synthase and PGP phosphatase catalyze the sequential synthesis of phosphatidylglycerol from cytidine-5'-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG) and glycerol-3-phosphate. PGP synthase and PGP phosphatase activities were characterized in rat heart mitochondrial fractions, and the effect of fatty acids on the activity of these enzymes was determined. PGP synthase was observed to be a heat labile enzyme that exhibited apparent Km values for CDP-PG and glycerol-3-phosphate of 46 and 20 microM, respectively. The addition of exogenous oleic acid to the assay mixture did not affect PGP synthase activity. PGP phosphatase was observed to be a heat labile enzyme, and addition of oleic acid to the assay mixture caused a concentration-dependent stimulation of PGP phosphatase activity. Maximum stimulation (1.9-fold) of enzyme activity was observed in the presence of 0.5 mM oleic acid, but the stimulation was slightly attenuated by the presence of albumin in the assay. The presence of oleic acid in the assay mixture caused the inactivation of PGP phosphatase activity to be retarded at 55 degrees C. Stimulation of PGP phosphatase activity was also observed with arachidonic acid, whereas taurocholic, stearic and palmitic acids did not significantly affect PGP phosphatase activity. The activity of mitochondrial phosphatidic acid phosphohydrolase was not affected by inclusion of oleic acid in the incubation mixture. We postulate that unsaturated fatty acids stimulate PGP phosphatase activity in rat heart.
Linxian, China, has one of the highest esophageal-cancer mortality rates in the world. In 1983, esophageal balloon-cytology screening was performed to identify subjects eligible for 2 nutrition-intervention trials in Linxian; 12,877 subjects had cytology slides which were satisfactory for diagnosis. Of the 12,649 subjects with squamous-cell diagnoses, 31% were normal by Chinese cytologic criteria; 38% showed hyperplasia; 21% showed dysplasia 1; 6% showed dysplasia 2; 2% showed near-cancer; and 2% showed cancer. Of the 1,471 subjects with columnar-cell diagnoses, 31% were normal; 44% showed hyperplasia; 16% showed dysplasia 1; 4% showed dysplasia 2; 2% showed near-cancer; and 3% showed cancer. Squamous dysplasia and cancer were more common among females than males, while columnar dysplasia and cancer showed male predominance. The prevalence of dysplasia and cancer of both cell types increased with age. The prevalence of squamous dysplasia was significantly higher than in earlier balloon-cytology screenings in Linxian, probably reflecting changes in cytologic classification.
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Acetic anhydride, dextran and monomethoxypolyethylene glycol and different modification methods were used for modification of L-asparaginase to maintain enzyme activity and completely remove its antigenicity. The results showed that the macromolecular modifiers PEG and dextran were better than the small molecular modifier acetic anhydride. For maintenance of enzyme activity and removal of antigenicity modification in the presence of substrate was better than absence of substrate and activated PEG2 was better than activated PEG1. When PEG2-L-asparaginase was modified in the presence of substrate, its antigenicity was completely removed, while more than 30% of native enzyme activity were still retained.
In 1983, intervention of precancerous lesion of esophagus was undertaken in the high risk area of esophageal cancer, Heshun Village, Linxian County. It had been expected that cancerous degeneration rate of esophageal dysplasia should be reduced by 50% so as the prevention of esophageal cancer could become possible. 6758 subjects of the general population aging from 40 to 65 were examined by esophageal exfoliative cytology, 1729 had marked dysplasia and 2411 had mild dysplasia of esophageal epithelium. Those with marked dysplasia were randomized into 3 groups to take their respective medication: antitumor B (Chinese herbs); retinamide (4-Ethoxycarbophenylretinamide) and placebo. The subjects with mild dysplasia were divided randomly into 2 groups for treatment by riboflavin and placebo. 95% of the subjects had taken 90% or more of the total medication for 3 years, at the end of which they were reexamined by esophageal exfoliative cytology. The reexamination rate was 94.1%. The incidence of esophageal cancer in the antitumor B group (3.9%) was reduced by 53% as compared with that of the placebo group (8.3%). This difference had statistical significant (means 2 = 7.672, P less than 0.05). The incidence of esophageal cancer in retinamide and riboflavin groups were reduced by 33.7% and 19% as compared with those of the control groups. The regression rate of dysplasia in the treatment groups were increased than that of the control groups. The above results showed that our hypothesis about the secondary prevention of esophageal cancer is correct. The intervention of precancerous lesion of the esophagus is effective in the prevention of esophageal cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
Hemin, having two carboxyl groups, was coupled with alpha-(3-aminopropyl)-omega-methoxypoly(oxyethylene) through the acid-amide bond formed with carbodiimide. The modified hemin catalyzed the peroxidase reaction in 1,1,1-trichloroethane using benzoyl peroxide or peroxides in unsaturated fatty acids as the hydrogen acceptor and leuco crystal violet as the hydrogen donor. A basic study on quantitative microanalysis of the lipid peroxides was attempted.
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Oleate has been shown previously to stimulate the in vitro activity of phosphatidylglycerol-phosphatase, an important enzyme in the cytidine-5'-diphosphate-1,2-diacyl-sn-glycerol pathway of phosphatidylglycerol and cardiolipin biosynthesis. In this study the in vivo effect of oleate on the biosynthesis of new phosphatidylglycerol and cardiolipin was investigated in the heart. Hearts were perfused for 60 min with Krebs-Henseleit buffer containing [1,3-3H]glycerol and 0.6 mM albumin in the absence or presence of 0.6 or 1.2 mM oleate. Total incorporation of radioactivity was higher in the oleate-treated hearts compared with controls and this was due to an exclusive incorporation of radioactive glycerol into the organic phase. Also, the radioactivity incorporated into phosphatidylglycerol and cardiolipin was higher in the oleate-treated hearts compared with controls; however, the increase was greater in hearts perfused with 0.6 mM oleate compared with 1.2 mM oleate, indicating that pathophysiological concentrations of oleate may attenuate the oleate-induced stimulation of glycerol incorporation into polyglycerophospholipids. The pool size of phosphatidylglycerol and cardiolipin were unchanged in oleate-perfused hearts compared with controls. To investigate if the biosynthesis of phosphatidylglycerol and cardiolipin via the cytidine-5'-diphosphate-1,2-diacyl-sn-glycerol pathway was authentically stimulated by oleate hearts were pulse labeled for 15 min with 0.1 mM [1,3-3H]glycerol and subsequently chased for 60 min with 0.1 mM glycerol in the absence or presence of 0.6 mM oleate in the perfusate. Radioactivity incorporated into phosphatidylglycerol and cardiolipin was unchanged compared with controls. Our data indicate that oleate increases the incorporation of exogenous glycerol into polyglycerophospholipids but not accelerate synthesis from prelabeled precursor pools. Accordingly, oleate does not appear to stimulate directly enzymes of the cytidine-5'-diphosphate-1,2-diacyl-sn-glycerol pathway in vivo.
This paper reports a 15-year follow-up study of 12,693 persons in Linxian, China, who were originally screened by esophageal balloon cytology in 1974. The purpose of the study was to evaluate the ability of esophageal balloon cytology to identify individuals at increased risk for developing esophageal cancer. Age, sex and cytologic diagnoses were obtained from the original 1974 records, and information on vital status, cancer experience and potential confounding risk factors was collected from interviews and medical abstracts in 1989. A total of 1,162 incident cases of esophageal cancer and 993 deaths due to esophageal cancer were identified and used in this analysis. The follow-up study showed that the risk of esophageal cancer incidence and mortality increased in parallel with the presumed severity of the 1974 Chinese cytologic diagnoses. After adjusting for potential confounding factors, the relative risks (and 95% confidence intervals) for esophageal cancer incidence, by cytologic diagnosis, were: normal, 1.00; esophagitis, 1.52 (1.07-2.14); hyperplasia, 1.17 (1.02-1.33); dysplasia 1, 1.53 (1.10-2.14); dysplasia 2, 1.89 (1.47-2.41); and suspicious for cancer, 5.77 (3.79-8.80). These results suggest that esophageal balloon cytology, as performed and interpreted in Linxian in 1974, successfully identified individuals at increased risk for esophageal cancer.