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Biomedical subjects

D Steinberg

Publications and source records attributed to D Steinberg.

At least 379 records · Page 21Linked to original sources
PubMed1966

Effects of dietary phytol and phytanic acid in animals.

Feeding of phytol in large doses (2-5% by weight in the diet) led to accumulation of phytanic acid in the mouse, rat, rabbit, and chinchilla, the degree of accumulation depending upon the level of dietary intake. The relative concentration of phytanic acid, expressed as a percentage of the total fatty acids, was as high as 20-60% in liver and 30-40% in serum. Phytenic acid, which may be an intermediate in the conversion of phytol to phytanic acid, also accumulated. When phytol was withdrawn from the diet, tissue and serum concentrations of phytanic acid fell rapidly, which indicates the ability of the normal animal to metabolize phytanic acid readily. At high dosages in the diet, phytol inhibited growth and caused death within 1-4 weeks. In the mouse, dietary phytanic acid and dietary phytol fed in equivalent amounts were of comparable toxicity. Accumulation of tissue phytanic acid occurred more rapidly when phytanic acid was fed than when phytol was fed in equal amounts. In none of the animals fed either phytol or phytanic acid were there any signs of neurological defects. Histologic examination of rats fed phytol showed some fat accumulation, glycogen depletion, and karyokinesis in the liver. There were no pathologic changes in the retina or in the peripheral and central nervous system such as those described in Refsum's disease.

Adrenal Glands↗
PubMed1966

Release of free fatty acids from Ehrlich ascites tumor cells.

Ehrlich ascites tumor cells release free fatty acids (FFA) during in vitro incubation in media that contain albumin. The released FFA are derived by lipolysis from endogenous lipid esters. Addition of glucose to the incubation medium greatly decreases the quantity of fatty acid released by the cells. Cyanide, which inhibits endogenous lipid oxidation but not lipolysis, increases the quantity of fatty acid released to media containing albumin and causes free fatty acid to accumulate in the cells in the absence of exogenous albumin. The release of fatty acid, either preformed or derived by lipolysis during prolonged incubations, occurs under conditions of net fatty acid uptake from the incubation medium. Net release of fatty acid from the cell occurs only when fatty acid-extracted albumin is present in the extracellular medium; extrapolation of the data suggests that net release will not occur under physiological conditions. It is postulated that free fatty acid uptake and release are independent processes, the direction of net fatty acid movement being determined by the relationship between cellular free fatty acid concentration (regulating efflux) and the molar ratio of free fatty acid to albumin in the extracellular medium (regulating uptake).

Animals↗
PubMed1966

Relationship between fatty acid and glucose utilization in Ehrlich ascites tumor cells.

Glucose greatly increased total free fatty acid (FFA) esterification by Ehrlich ascites tumor cells. However, the FFA concentration of the cells was not altered. Less exogenous FFA was oxidized to CO(2) at any given extracellular FFA:albumin molar ratio when glucose was available, but increasing amounts of radioactive CO(2) were produced as the FFA:albumin molar ratio was raised, even in the presence of glucose. It is suggested that glucose, by providing either energy or an excess of triose acceptor for fatty acid esterification, stimulated FFA uptake only indirectly, by increasing the utilization of FFA subsequent to initial uptake from the medium, i.e., by increasing the turnover rate of the cellular FFA pool. Availability of glucose decreased the oxidation of endogenous lipid radioactivity and the depletion of endogenous lipid ester radioactivity. Most of the radioactivity utilized was derived from phospholipids, and depletion of phospholipid radio-activity was spared when glucose was available. Depletion of cellular total lipid ester also was spared in the presence of glucose. Availability of FFA did not decrease total glucose uptake or its oxidation to CO(2). Glucose utilization by these cells appears not to be regulated by FFA availability in the manner that Randle and coworkers described for muscle.

Animals↗
PubMed1966

Metabolism of phytol-U-14C and phytanic acid-U-14C in the rat.

The metabolism of uniformly-labeled (14)C-phytol, (14)C-phytenic acid, and (14)C-phytanic acid was studied in the rat. Conversion of both phytol and phytenic acid to phytanic acid was demonstrated. Tracer doses of phytol-U-(14)C given orally were well absorbed (30-66%), and approximately 30% of the absorbed dose was converted to (14)CO(2) in 18 hr. After intravenous injection, 20% appeared in (14)CO(2) in 4 hr. Phytanic acid-U-(14)C given intravenously was oxidized at a comparable rate (22-37% in 4 hr) and was as rapidly oxidized as palmitic acid-1-(14)C (21% in 4 hr). Metabolism of these substrates was also studied in rats previously maintained on a diet containing 5% phytol by weight, which causes accumulation of phytanic acid, phytenic acid, and, to a lesser extent, phytol in blood and tissues. Despite the large body pools of preformed, unlabeled substrate in these animals, the fraction of an administered dose of phytol-U-(14)C or phytanic acid-U-(14)C converted to (14)CO(2) was not significantly diminished. These studies indicate that the rat has an appreciable capacity to degrade the highly branched carbon skeleton of phytol and its derivatives. Twenty-four hours after administration of phytol-U-(14)C, the lipid radioactivity remaining in the body was widely distributed among the tissues, highest concentrations being found in liver and adipose tissue. Four hours after intravenous administration of phytanic acid-U-(14)C, all of the major lipid classes in the liver contained radioactivity, most in triglycerides and phospholipids and least in cholesterol esters and lower glycerides. There was no demonstrable incorporation of mevalonate-2-(14)C or acetate-1-(14)C into liver phytanic acid when they were given intravenously to a rat previously fed phytol. Endogenous biosynthesis, if it occurs at all, must be extremely limited.

Adipose Tissue↗
PubMedDate not supplied

Antibacterial effect of chlorhexidine on bacteria adsorbed onto experimental dental plaque.

The most common method used to examine the antibacterial effect of antiplaque agents is the minimal inhibitory concentration (MIC) method, which is tested on bacteria in suspensions. Examining the antibacterial effect on bacteria adsorbed onto dental surfaces models is not as popular, although it is clear that such models reflect the conditions in the oral cavity far more accurately than the conventional MIC method. The antibacterial effect of chlorhexidine (CHX) on bacteria adsorbed onto experimental dental plaque model was investigated. Hydroxyapatite beads were coated with human saliva. Next, cell-free fructosyltransferase (FTF) and glucosyltransferase (GTF) were adsorbed onto the beads, and sucrose was added to allow the synthesis of polysaccharide by the surface-bound enzymes. Following adsorption of Streptococcus sobrinus to the experimental dental plaque (EDP), the EDP was exposed to CHX at concentrations between 0.008 to 0.0002% at pH values of 5.5, 6.5, and 7.5. After 150 min incubation, growth of the adsorbed bacteria was measured by their incorporation of 3H-uridine or 3H-thymidine. Comparison of bacterial growth on the EDP with that in suspension showed that the surface-bound bacteria were less sensitive to CHX than were the bacteria in suspension. At all tested CHX concentrations, the antibacterial effect was independent of pH. In addition, under our experimental conditions, the use of 3H-uridine as an indicator of bacterial viability proved to be more sensitive than 3H-thymidine. The antibacterial effect of an agent in a model closely mimicking the tooth surface should generate results that are more relevant to the in vivo conditions than are conventional methods, thus bearing significant information concerning clinical applications of CHX.

Adult↗
PubMedDate not supplied

The oxidative modification hypothesis of atherosclerosis: does it hold for humans?

This review suggests that oxidation of LDL is an important, if not obligatory, event in atherogenesis. The important clinical corollary is that inhibition of oxidation can inhibit atherosclerosis independent of lowering plasma cholesterol levels. This article surveys the extensive data supporting the presence of oxidized LDL in vivo in animal models; the many studies demonstrating that inhibition of oxidation by pharmacologic and/or genetic manipulations retards atherogenesis; the data in humans that supports a role for oxidation of LDL; and the results of intervention trials with antioxidant vitamins. Limitations of these trials that may have led to inconclusive results to date are discussed, and what this may mean for the oxidation hypothesis. The oxidation hypothesis is still viable, but a great deal needs to be learned in order to design the appropriate clinical trials to properly test the importance of oxidation in the pathogenesis of atherosclerosis in humans.

Animals↗
PubMedDate not supplied

Caries experience, periodontal treatment needs, salivary pH, and Streptococcus mutans counts in a preadolescent Down syndrome population.

The prevalence of dental caries and periodontal treatment needs in an institutionalized population with Down syndrome was examined and the relationship between caries prevalence, salivary pH, and salivary levels of Streptococcus mutans was studied. Thirty-two children with Down syndrome, aged 8 to 13, were compared with two control groups of similar age ranges: healthy children and non-Down mentally retarded (MR) children living in the same institution as the Down syndrome population. The gender ratio mixtures in each group also matched the study sample. Caries experience as indicated by decayed, missing, and filled surfaces (DMF-S) showed significantly lower mean scores for the Down syndrome group compared with both control groups. A similar pattern was found when evaluating the mean numbers of decayed surfaces. Streptococcus mutans counts, expressed as number of colony-forming units on mitis salivarius agar plates among the Down syndrome group, were the lowest, although not statistically significant compared with the counts of the healthy children. Both groups had bacterial counts which were significantly lower than those of the MR group. Significant differences between the two institutionalized groups and the healthy group were recorded for the salivary pH levels. The periodontal treatment needs as evaluated by the Community Periodontal Index of Treatment Needs showed significant difference between the MR group versus both the healthy population and the Down syndrome group. On the whole, 84% of the Down syndrome children were cariesfree.

Adolescent↗
PubMedDate not supplied

The anticariogenic effect of amine fluorides on Streptococcus sobrinus and glucosyltransferase in biofilms.

Dental caries is a chronic infectious disease caused by the accumulation of bacterial plaque (biofilm) on tooth surfaces. Antibacterial agents, in addition to other preventive measures, can control dental plaque accumulation. Amine fluorides (AmF) are known anticaries agents for over 30 years. The purpose of our study was to assess the adsorption and desorption of AmF to experimental dental biofilm and to evaluate the effect of AmF on Streptococcus sobrinus 6715 and glucosyltransferase (GTF) activity in experimental dental biofilms. The experimental plaque model used in this study consists of hydroxyapatite beads coated with human saliva (sHA), followed by adsorption of S. sobrinus and synthesis of in situ polysaccharides. Our results show that the viability of S. sobrinus in biofilm decreased as the concentration of AmF and chlorhexidine (CHX) increased. The concentration of AmF and CHX required to kill S. sobrinus adherent to sHA is about 100 times greater than the concentration required to kill the same amount of planktonic bacteria. Adsorption of AmF to surfaces was more than 90% and the desorption of AmF from our experimental model was limited. Pre-adsorption of AmF on the surface increased adhesion of S. sobrinus but also resulted in surface killing of the adsorbed bacteria. At low concentrations AmF increased GTF activity in solution by about 10%, but at concentrations above 0.1 mM it inhibited GTF activity. Inhibition of GTF on the surface required about 100 times more AmF than in solution. Our results show that AmF retains its anticariogenic effects in solution and in biofilm systems.

Adult↗