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Biomedical subjects

R Albrecht

Publications and source records attributed to R Albrecht.

At least 19 recordsLinked to original sources

Effect of phenoclor DP6 on enzyme-altered foci and lipid peroxidation in livers of aflatoxin B1-initiated rats.

This study investigates the capacity of phenoclor DP6 to promote aflatoxin B1 (AFB1)-induced putative preneoplastic foci in the liver. In male Sprague-Dawley rats pretreated with AFB1 (ip injection of 1 or 2 mg/kg body weight once weekly for 3 consecutive wk) and given a diet containing 50 ppm phenoclor DP6 for 11 days, the number of area of putative liver preneoplastic lesions were increased approximately four-fold as indicated by the number and gamma-glutamyl transpeptidase activity of enzyme-altered foci; this change was also accompanied by an increase in hepatic microsomal lipid peroxidation and a decrease in Se-glutathione peroxidase and superoxide dismutase activities. The results indicate that phenoclor DP6 exerts a promoting effect in AFB1-initiated rats.

Aflatoxin B1

Effect of prototypic polychlorinated biphenyls on hepatic and renal vitamin contents and on drug-metabolizing enzymes in rats fed diets containing low or high levels of retinyl palmitate.

Two groups of weanling male Sprague-Dawley rats fed a diet supplemented with either 0.6 or 6 retinol equivalents/g diet were each separated into three further groups receiving 300 mumol 2,2',4,4',5,5'-hexachlorobiphenyl/kg body weight, 300 mumol 3,3',4,4'-tetrachlorobiphenyl kg/body weight or vehicle only (corn oil). Only the coplanar (3,4)2Cl congener caused a slight reduction in food intake, thymic atrophy and led to a significant decrease in the liver vitamin A storage. The vitamin A lost by the liver was approximately the same in both dietary groups; however an increased renal accumulation of vitamin A was observed in the high vitamin A group. Serum retinol was reduced by (3,4)2Cl treatment but remained unchanged by (2,4,5)2Cl exposure. Total amounts of ascorbic acid and its oxidation products were increased in the liver and in the kidney by both xenobiotics while niacin and thiamine concentrations were lowered by (3,4)2Cl only. Microsomes from vitamin A-deficient rats exhibited a marked decrease in the anisotropy parameter. After (2,4,5)2Cl exposure, an increase in membrane fluidity was observed linked to a decrease in cholesterol/phospholipid (C/P) ratio. Treatment with (3,4)2Cl caused a significant decrease in the index of fluorescence polarization only in the low vitamin A group even if the C/P ratio was enhanced in both dietary groups. This study shows that the polychlorinated biphenyl with the 3-methylcholanthrene-type pattern of induction of cytochrome P-450 has more profound effects on B group vitamins and particularly vitamin A homeostasis than does the phenobarbital-type inducer. Moreover, this situation, which has been found to be similar to that in vitamin A deficiency, is not ameliorated by a high dietary vitamin A intake.

Animals

Dietary restriction decreases thiobarbituric acid-reactive substances generation in the small intestine and in the liver of young rats.

This study investigated the influence of dietary restriction on thiobarbituric acid-reactive substances (TBARS) contents and on the intracellular antioxidant defence system in the small intestine or liver of young rats. Four weeks of diet restriction (-40%) lowered the TBARS level in both organs. No variations were found for the superoxide dismutase and catalase activities; only liver seleno-dependent glutathione peroxidase was enhanced by the restriction. The protection appeared more marked in the intestine than in the liver, and would be dependent on glutathione concentration.

Animals

Activation-dependent changes in human platelet PECAM-1: phosphorylation, cytoskeletal association, and surface membrane redistribution.

PECAM-1 is a recently described member of the immunoglobulin gene (Ig) superfamily that is expressed on the surface on platelets, several leukocyte subsets, and at the endothelial cell intracellular junction. Recent studies have shown that the extracellular domain of PECAM-1, which is comprised of 6 Ig-like homology units, participates in mediating cell-cell adhesion, plays a role in initiating endothelial cell contact, and may later serve to stabilize the endothelial cell monolayer. PECAM-1 also has a relatively large 108 amino acid cytoplasmic domain, with potential sites for phosphorylation, lipid modification, and other posttranslational events that could potentially modulate its adhesive function or regulate its subcellular distribution. Virtually nothing is known about the contribution of the intracellular region of the PECAM-1 molecule to either of these cellular processes. Using human platelets as a model, we now demonstrate that PECAM-1 becomes highly phosphorylated in response to cellular activation, and coincident with phosphorylation associates with the cytoskeleton of activated, but not resting, platelets. The engagement of PECAM-1 with the platelet cytoskeleton enables it to move large distances within the plane of the membrane of fully-spread, adherent platelets. This redistribution may similarly account for the ability of PECAM-1 to localize to the intracellular borders of endothelial cells once cell-cell contact has been achieved.

Antigens, Differentiation, Myelomonocytic

Peptidergic innervation of the Bursa Fabricii: interrelation with T-lymphocyte subsets.

In birds, B-lymphocytes mature in a special immune organ, the Bursa Fabricii. This organ thus offers unique possibilities for the study of the microenvironment of B-lymphocyte differentiation. We previously reported tachykinin-, vasoactive intestinal peptide-, calcitonin gene-related peptide- and galanin-immunoreactive (ir) fibres in the chicken bursa. As judged from light microscopic studies, each of the peptides was found in fibres contacting B-lymphocytes. Vasoactive intestinal peptide-ir fibres contacted macrophages. Now, we demonstrate neuropeptide Y, indicating the sympathetic nervous system, in fibres associated with arteries, not entering the follicles. CD4- and CD8-positive T-lymphocytes were dispersed in bursal follicles and the connective tissue, most densely in subepithelial regions. We could not find close apposition of fibres with either T-cell subset. We conclude that the potential neuro-immune axis in the Bursa Fabricii may represent a neuro-B-cell-link with only indirect participation of T-lymphocytes. The sympathetic input may influence the bursal microenvironment primarily by regulating the blood supply.

Animals

A time course investigation of vitamin A level and lipid composition of the liver endoplasmic reticulum in rats following treatment with congeneric polychlorobiphenyls.

The drug metabolizing enzyme activities, the vitamin A content and the fatty acid composition in the endoplasmic reticulum membrane were studied in rat liver after a single injection of the polychlorobiphenyls (PCBs) 3,3',4,4'-tetrachlorobiphenyl [(3,4)2Cl] or 2,2',4,4',5,5'-hexachloro-biphenyl [(2,4,5)2Cl], 300 mumol/kg each. The microsomal vitamin A level was markedly lowered 3 days after treatment with (3,4)2Cl, a coplanar type inducer of cytochrome P-450. A marked increase in microsomal AHH and UDPGT activities occurred within 3 days after injection of (3,4)2Cl whereas (2,4,5,)2Cl treatment enhanced APDM activity only. Arachidonic, stearic and linoleic acid microsomal contents were enhanced by the two congeners. (3,4)2Cl caused the proportion of docosahexaenoic acid to decrease. No highly significant correlation was found between the vitamin A content and lipid components in the microsomal membrane. However, the vitamin A level was inversely related to the activities of drug metabolizing enzymes induced by coplanar compounds (cytochrome P-450 towards benzo[a]pyrene and UDP glucuronosyl transferase towards 4-nitrophenol).

Animals

Lipid peroxidation of rat liver microsomes membranes related to a protein deficiency and/or a PCB treatment.

In this study, we investigated the influence of protein deficiency on lipid peroxidation (LP) and cellular defense systems against oxidative damage in control or polychlorinated biphenyl (PCB) treated rats. Rats were fed either a standard diet (22% casein) or a low protein diet (3.5% casein) for 1, 2 and 6 weeks. Five days prior to killing, one half of the animals were given a single i.p. injection of Phenoclor DP6 (50 mg/kg body weight). In protein deficient rats, liver vitamin E was depressed and ascorbate level was lowered. Total and selenium-dependent glutathione peroxidases (GSH-Px) activities were decreased whereas glutathione reductase (GSH-red) was enhanced. Enzymatic and non enzymatic LP ('spontaneous' or with ADP-Fe2+) were increased. Phenoclor DP6 treatment enhanced liver ascorbate concentration. Microsomal LP was increased. Total and selenium-GSHPx remained unmodified while GSH-red was increased. Liver glutathione and alpha-tocopherol contents appeared to be independent of the PCB injection. Our data suggest that low protein intake and PCB exposure may reduce liver defensive protection against electrophilic species.

Animals

[Mucosa protection--an assessable value? An experimental study in rats].

Reduced mucosaprotection is a main factor for development of peptic ulcer disease. The quantity is difficult to estimate. We did it by measuring the acid output as the aggressive factor and we sized the resulting mucosalesions. In the gastric corpus we could not find any change in mucosaprotectionindex after cimetidine, pirenzepine and vagotomy. But in the duodenum protection was increased after pirenzepine and vagotomy.

Animals

Probable exclusion of juvenile neuronal ceroid lipofuscinosis in a fetus at risk: an interim report.

In a family with two children affected by juvenile neuronal ceroid lipofuscinosis (JNCL) an attempt was made at the prenatal diagnosis of the disorder. The following tissues from the fetus at risk were investigated by electron microscopy and were found to be free of fingerprint profiles and curvilinear bodies, typical for JNCL: uncultivated amniotic fluid cells, lymphocytes isolated from fetal blood, and fetal skin biopsy specimens. The child was born at the 34th week of gestation and was clinically normal at the age of 15 months. Postnatally, lymphocytes (isolated at the age of 6 and 15 months) and skin tissue (taken at the age of 15 months) were found to be morphologically normal. It is highly unlikely that the child is affected but definite proof of the absence of JNCL remains difficult at this age.

Amniocentesis

Cardiovascular correlates of type A behavior components during social interaction.

This study examined the cardiovascular (CV) correlates of the primary Type A behavior components during social interactions. Brief dialogues were created to role-play (RP) stereotypic Type A and Type B ways of responding to three common social situations designed to elicit hostility (H), time-urgency (T), and competition (C). Situations and dialogues were validated by independent raters. Thirty undergraduate students were identified as Type A and 30 as Type B, with 15 males and 15 females in each group. Subjects were provided scripts for each of the six experimental RPs and rehearsed them prior to the CV assessment. Measures of systolic and diastolic blood pressure (SBP, DBP) and heart-rate (HR) were obtained during an adaptation period and during each RP. Analyses of the "A" (i.e. H, T, C) versus "B" (i.e. non-H, non-T, non-C) RPs indicated that DBP (p less than 0.03) and HR (p less than 0.002) were higher during the H as compared with non-H RP. Significantly higher SBP was observed in the T as compared with the non-T RP (p less than 0.04). No CV differences were observed in the comparison of the C and non-C RPs. Analyses comparing the three "Type A" RPs revealed higher SBP during H and T RPs, as compared with the C RP (p less than 0.003). Effects of subject Type (i.e. A/B) were not obtained in any analysis. These findings indicate that hostile and time-urgent social interactions are associated with significant increases in CV arousal which are independent of overall Type status.

Adult

Effects of prototypic PCBs on benzo[a]pyrene mutagenic activity related to vitamin A intake.

The effects of vitamin A dietary intake (2 and 20 IU */g of food) on the mutagenic activity of benzo[a]pyrene (B(a)P) toward Salmonella typhimurium (TA98) were studied either in control rats or in animals treated by the PCB congeners 2,4,5,2',4',5'-hexachlorobiphenyl [2,4,5)2Cl) and 3,4,3',4'-tetrachlorobiphenyl [3,4)2Cl). (3,4)2Cl (a planar compound) strongly increased B(a)P monooxygenase (B(a)PMO) activity and glutathione transferase, (2,4,5)2Cl (a non-planar PCB) was a strong inducer of epoxide hydrolase and a weak inducer of B(a)PMO. Enzyme induction was not modified by changes in vitamin A dietary intake. A higher mutagenic effect was observed in the (3,4)2Cl group than in the (2,4,5)2Cl one. This could be related to the specific form of cytochrome P-450 induced by (3,4)2Cl. In the untreated animals, the activation of B(a)P was higher in the 2-IU group than in the 20-IU one. Conversely, in PCB-treated rats the mutagenic activity of B(a)P was higher in the 20-IU group than in the 2-IU one. PCB induction increased the liver content of vitamin C in both the 2-IU and the 20-IU groups but only increased the glutathione levels in the 2-IU groups. This suggests that glutathione content in cellular fractions may be one of the determining parameters for the mutagenic activity of B(a)P.

Animals

[Gastric perfusion in the rat--a method for determining gastric secretion].

The response of the 3 postulated receptors in the parietal cell was investigated by means of a perfusion model in the rat. It was compared the effect of cimetidine and atropine on pentagastrin, histamine and carbachol stimulated gastric acid secretion with a control group. Atropine blocked the carbachol stimulation totally but did not effect pentagastrin and histamine stimulation. Cimetidine inhibited all stimulations. This method is a model for study of drugs influences of the gastric secretion.

Animals

[Syndrome following injury of the ventromedial hypothalamic nucleus (VMH syndrome) and its relation to increased secretion of gastric acid (hyperchlorhydria)--an experimental study with rats].

In rats a stereotactic electrocoagulation of the Nucleus ventromedialis hypothalami (NVM) leads to a VMH syndrome (ventromedial hypothalamic syndrome) with hyperphagia, adiposity, and hyperinsulinaemia. A less known fact in this connection is the increased secretion of gastric acid (hyperchlorohydria). We could prove that the basal gastric secretion increases after NVM lesions by two times (from 18 mumol H+/hr to 37 mumol H+/hr) and that this hyperchlorohydria can be removed by a vagotomy. From this fact one can derive conclusions concerning the acute gastric mucous secretion after brain lesions with regard to their pathogenesis and therapy.

Animals

[Increased cholinergic stimulating gastric secretion after truncal vagotomy in rats].

The reasons of the relapses after vagotomy are not clarified completely. The reactivity of the 3 postulated receptors in the parietal cell was investigated by means of a perfusion model in the rat in a control group and after truncus vagotomy 28 days before the experiment. Not any difference was shown between the control group or the vagotomy group after histamine and pentagastrin stimulation. A significant greater secretion (!) with negative insulin test was observed in the vagotomy group after carbachol stimulation.

Animals

The effect of dietary imbalances on the activation of benzo[a]pyrene by the metabolizing enzymes from rat liver.

Male Sprague-Dawley rats (70-80 g) were fed ad libitum a standard control diet (22% casein, 5% lard), or a high lipid diet (30% lard) or a low protein diet (6% casein) or a standard diet containing 50 ppm phenoclor DP6. After 6 weeks on these diets, the cytochrome P-450 microsomal content, the benzo[a]pyrene monooxygenase (BaP-MO) and the epoxide hydrolase (EH) were assayed. The formation of mutagenic B(a)P metabolites which covalently bind with DNA was compared. The activity of BaP-MO and of EH were increased by the high lipid diet (+27% and 106% respectively) and by the phenoclor DP6 treatment (+63% and 400% respectively), compared to the standard diet. In animals fed a low protein diet the BaP-MO was decreased (-34%) and the EH activity was strongly increased (+262%) compared to those fed a standard diet. All experimental diets increased both the activation of BaP to metabolites able to bind DNA and the mutagenicity of BaP versus TA98 Salmonella typhimurium strain. It was concluded that dietary imbalances can be considered as a factor in chemical carcinogenesis.

Animals