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B Anderstam

Publications and source records attributed to B Anderstam.

32 records · Page 2Linked to original sources
PubMed1996

Influence of peritoneal dialysis solutions with glucose and amino acids on ingestive behavior in rats.

Continuous ambulatory peritoneal dialysis (CAPD) is often associated with malnutrition; reduced intake of nutrients due to anorexia is an important factor. The glucose load from glucose-based peritoneal dialysis (PD) solutions and amino acids from amino acid-based solutions may favor suppression of the appetite. To study this matter we used a new experimental model in free-moving, unstressed male Wistar rats (300 to 350 g) with feeding catheters channeled from the top of the skull to the oral cavity. When the rats recovered from surgery they were tested under standardized conditions by giving them an intraoral infusion (1 ml/min) of a solution containing 342 g/liter of the sucrose or 97 g/liter protein solutions while recording the time (volume) of ingestion. Control rats consumed 18.8 +/- 0.9 ml of the sucrose and 39.8 +/- 0.8 ml of the protein solutions. Injections of PD solutions with 13.6, 22.7, and 38.6 g/liter of glucose reduced the ingestion of sucrose by 12.4%, 23.6% and 36.1%, respectively, but did not affect the ingestion of protein. Injections of 30 ml of PD solutions containing 11, 18 and 31 g/liter of amino acids reduced the ingestion of both sucrose by 9.7%, 17.1% and 33.2% and of protein by 13.5%, 25.9% and 33.1%, respectively. We conclude that in our experimental model, the inhibition of appetite caused by peritoneal solutions containing glucose or amino acids seems to be specific for each nutritional constituent and not simply an effect of hyperosmolality or large filling volumes.

Adaptation, Physiological↗
PubMed1996

Evidence of taurine depletion and accumulation of cysteinesulfinic acid in chronic dialysis patients.

Methionine, taurine and cysteinesulfinic acid (CSA) were determined by reversed-phase high-performance liquid chromatography (RP-HPLC) in plasma from ten patients treated with hemodialysis (HD) and eight patients treated with continuous ambulatory peritoneal dialysis (CAPD). The patients' data were compared with data obtained from ten healthy controls. Significant reductions in plasma taurine levels were observed in the HD patients (34 +/- 13 mumol/liter, mean +/- SD) and the CAPD patients (47 +/- 12 mumol/liter) compared to the controls (66 +/- 5 mumol/liter), while the CSA levels were markedly higher in the HD patients (9.1 +/- 2.8 mumol/liter) and the CAPD patients (9.1 +/- 2.4 mumol/liter) than in the controls (0.79 +/- 0.15 mumol/liter). A single HD treatment significantly reduced the plasma taurine and CSA concentrations (P < 0.01 and P < 0.001), respectively. The plasma methionine levels were normal in both patient groups. The finding of a low plasma taurine level and a large accumulation of CSA suggests that the metabolic conversion of CSA to taurine is impaired in uremic patients and this metabolic abnormality may cause taurine depletion.

Adolescent↗
PubMed1996

Thiols, recA induction and radiosensitivity in Escherichia coli.

Induction by gamma-radiation, UV radiation or hydroxyurea of RecA gene product synthesis in Escherichia coli, monitored as beta-D-galactosidase in recA-lacZ fusion strains, was shown to be inhibited if 2-mercaptoethylamine (MEA) was added before treatment with the inducing agents. If cysteine (Cys) at low concentrations was added at the same time as MEA it counteracted the action of MEA. The effect of MEA may be described as a competitive inhibition of an inducing or conducting effect of Cys. In E. coli GE499 (uvrA+), complete inhibition by 30-mmol dm-3 MEA of recA induction was associated with about five times higher radio-resistence. Both of these effects of MEA were completely reversed by 0.3-mmol dm-3 Cys. As shown in parallel experiments with E. coli GE500 (uvrA-), these effects of MEA and Cys were shown to be independent of excision-repair proficiency. Treatment of bacteria with MEA and/or Cys was shown not to lead to increased intracellular concentrations of these thiols. Instead, treatment with them appeared to provoke conspicuous increases in glutathione levels, which are, however, probably not directly involved in the studied action of MEA and Cys.

Cysteine↗
PubMed1996

Middle-sized molecule fractions isolated from uremic ultrafiltrate and normal urine inhibit ingestive behavior in the rat.

Uremic patients with suppressed food intake may regain appetite soon after starting dialysis, presumably because of the removal of one or more toxic factors that suppress appetite. To investigate this matter, this study used a new experimental model in free-moving, unstressed male Wistar rats (300 to 350 g) with feeding catheters channeled from the top of the skull to the oral cavity. When the rats recovered from surgery, they were tested under standardized conditions by being given an intraoral infusion (1 mL/min) of a 1 M sucrose solution or a 97 g/L protein solution or a mixed solution of carbohydrate, protein, and fat (Fortimel (Nutricia Nordica AB, Stockholm, Sweden)) while the time (volume) of ingestion was recorded. Solutions to be tested for their ability to inhibit ingestion were injected intraperitoneally (lp) and the intraoral infusion was started 20 min later. Plasma ultrafiltrate was collected from end-stage renal failure patients by isolated ultrafiltration at the beginning of their first hemodialysis and pooled. Ultrafiltrate was also obtained by filtering pooled plasma from healthy volunteers in vitro, using the same type of dialyzer and cellulose acetate membranes as those used in the uremic patients. Morning urine samples from healthy volunteers were pooled and subjected to the same in vitro filtration procedure as the normal plasma. Intraperitoneal injection of 20 mL normal ultrafiltrate had no effect on sucrose ingestion, whereas injection of 20 mL uremic ultrafiltrate reduced the ingestion of sucrose solution by 23% and the ingestion of Fortimel by 17%. Ten mL of ultrafiltrate from normal urine reduced the sucrose intake by 42%. The pooled ultrafiltrates from normal and uremic plasma and normal urine were subjected to molecular filtrations using a series of membranes with known cut-off points. The filtrations yielded four concentrated fractions with molecular weight ranges of 0.1 to 0.5 kilodaltons (kd), 0.5 to 1 kd, 1 to 5 kd, and 5 to 10 kd, respectively; the plasma fractions were concentrated a factor of about 25:1 and the urine fractions by about 15:1. After an ip injection of 2 mL of each concentrated plasma fraction, only the 1 to 5 kd fraction from the uremic ultrafiltrate inhibited sucrose intake, whereas the corresponding fraction from the normal ultrafiltrate had no effect. After injection of 1, 3, and 5 mL of the concentrated fractions of uremic ultrafiltrate, a dose-dependent inhibition of sucrose intake was achieved with the 1 to 5 kd fraction and, to a lesser extent, with the 5 to 10 kd fraction. Intraperitoneal injection of 0.5, 1.0, and 2 mL of the concentrated 1 to 5 kd fraction, but not of the other fractions from normal urine, also resulted in a dose-dependent inhibition of sucrose intake. The 1 to 5 kd fractions from the uremic ultrafiltrate and the normal urine ultrafiltrate also inhibited protein intake in a dose-dependent manner. These results suggest that one or more toxic compounds in the middle-molecule weight range, which are normally excreted in the urine, accumulate in uremia and suppress food intake.

Animals↗
PubMed1995

Diet-independent suppression of ingestive behavior by cholecystokinin octapeptide and amino acids.

Male rats consumed much more of an intraorally administered mixed protein, fat and carbohydrate solution than of a carbohydrate solution. Injection of cholecystokinin octapeptide (CCK-8, 0.6-5.0 microgram) suppressed intake of both solutions, but the CCK-A receptor antagonist L-364, 718 (20-40 micrograms) facilitated only carbohydrate intake. Blood levels of CCK-8 were higher after intake of the carbohydrate than the mixed solution. Blood levels of isoleucine, leucine, lysine, threonine, valine, and tryptophan increased only after intake of the mixed solution. Injection of these amino acids suppressed intake of both solutions. Blood levels of amino acids were also less after the seventh than after the first session ingesting the mixed solution. Treatment with CCK-8 or amino acids inhibits intake of any diet, but when secreted endogenously, these signals may terminate the meal in a diet-dependent manner.

Amino Acids↗
PubMed1992

Lipid peroxide levels in a murine adenocarcinoma exposed to hyperthermia: the role of glutathione depletion.

Increased lipid peroxide levels were obtained 1 h after a 60-min 43 degrees C hyperthermia treatment of a solid murine C3H mammary adenocarcinoma, grown subcutaneously in the hind paws of mice. Previous work from our group revealed that this heat treatment depletes the intracellular glutathione (GSH) content in this tumor. To investigate GSH depletion as one tentative mechanism behind the increased lipid peroxide levels obtained, we also measured the formation of lipid peroxidation products after extensive DL-buthionine-S,R-sulfoximine (BSO)-induced GSH depletion. The lipid peroxide effect provoked by BSO was less than that of the 60-min hyperthermia treatment. We therefore propose that the increased lipid peroxide levels induced by heat treatment do not correlate primarily with the observed decrease in GSH levels. Furthermore, in thermotolerance-induced tumors, lipid peroxide levels after a second heat treatment were observed to increase concomitantly with the cessation of thermotolerance. Lipid peroxide levels were also studied in liver, lung, and heart. Following BSO treatments, and up to 2-fold increase was observed in these organs in non-tumor-bearing mice. It was also observed that the intrinsic lipid peroxide levels in these organs from tumor-bearing mice were approximately 1.5- to 4-fold higher in comparison with non-tumor-bearing mice, thus indicating a systemic effect of the tumor implant.

Adenocarcinoma↗
PubMed1991

In vivo hemoglobin dosimetry of malonaldehyde and ethene in mice after induction of lipid peroxidation. Effects of membrane lipid fatty acid composition.

Hemoglobin (Hb) adduct determination by the N-alkyl Edman method was used for in vivo dosimetry of endogenously formed malonaldehyde (MA) and ethene in mice fed diets with different fatty acid composition and induced for lipid peroxidation with carbon tetrachloride (CCl4). In order to amplify lipid peroxidation animals were pretreated with phenobarbital (PB) and the glutathione-depleting agent DL-buthionine-(S,R)-sulfoximine (BSO). Non-treated animals raised on different diets were used as controls. Lipid peroxidation products in liver were measured as 2-thiobarbituric acid reactive compounds (TBA-C). Livers from control mice fed a soya oil based diet (rich in polyunsaturated fatty acids, diet S) showed approximately 6.5-fold higher levels of TBA-C than those from animals raised on a coconut oil based diet (mostly saturated fatty acids, diet C). The level of adducts of MA to Hb, determined as N-(3-hydroxypropyl)valine, was approximately 1.5-fold higher in animals from diet S than in animals raised on diet C. The highest increases in the levels of TBA-C and MA adducts were obtained after a simultaneous treatment of the animals with PB, BSO and CCl4. The increases of TBA-C were 1.3-fold (diet C) and 1.7-fold (diet S). The corresponding increases of MA-Hb adduct levels were 1.3- and 1.6-fold respectively, indicating an increased susceptibility of mice fed diet S to lipid peroxidation. The level of adducts from ethene, determined as N-(2-hydroxyethyl)valine, was also higher in mice from diet S than in animals fed diet C, when all treatment groups were considered. The difference was, however, only slightly significant (P less than 0.02). No difference between control and CCl4-treated animals, with regard to the ethene-Hb adduct, was found. Our results validate the use of Hb dosimetry for monitoring the effects of factors known to influence lipid peroxidation induced in vivo.

Animals↗
PubMed1989

Incorporation of [3H]acetate into the membrane lipids of a murine tumour during the development of thermotolerance.

The incorporation of [3H]acetate into the membrane lipids of a C3H mammary adenocarcinoma, grown s.c. in the hind paw of CBA mice, was followed to estimate the effects on the de novo synthesis of membrane lipids after hyperthermic treatments. Thermotolerance developed in response to a heat treatment at 43 degrees C for 20 min, as verified through growth rate studies of tumours exposed to fractionated heat treatments. Our results show that, during the development of thermotolerance, the relative rates of incorporation of [3H]acetate into the major lipid classes of the tumour cell membranes change significantly. The de novo synthesis of phospholipids decreased while that of cholesteryl esters plus triglycerides increased. The incorporation of [3H]acetate into cholesterol remained constant. Consequently, the ratio [3H]cholesterol/[3H]lecithin increased significantly during the development of thermotolerance. When the incorporation of [3H]acetate was followed 72-96 h after the heat treatment, i.e. at the interval at which heat resistance was observed to approach that of control tumours, the incorporation into cholesterol was significantly reduced while incorporation into phospholipids increased to control levels. Thus, the ratio [3H]cholesterol/[3H]lecithin was significantly lower, when compared to that of control tumours. The functional relationship between the heat-induced changes in the de novo synthesis of membrane lipids and the development of thermotolerance is discussed with regard to a mechanism based on homeoviscous adaptation of the membranes.

Acetates↗
PubMed1987

Heat-induced changes in the incorporation of [H3]acetate in membrane lipids.

The effects of heat treatments at temperatures from 42 to 47 degrees C on the rate of incorporation of [3H]acetate into different classes of lipids have been studied in V-79 Chinese hamster cells. Thermotolerance induction and subtoxic heat treatments decreased the incorporation of [3H]acetate into phospholipids and caused the ratio [3H]cholesterol/[3H]phospholipids to increase several fold, and a positive correlation between heat dose and the ratio [3H]cholesterol/[3H]phospholipids was obtained for subtoxic hyperthermic treatments. The duration of this hyperthermic effect on the incorporation of [3H]acetate into the different lipid fractions was followed in pulse-label experiments. The highest increase of the ratio [3H]cholesterol/[3H]phospholipids was obtained during the first 24 h, but a significant elevation was also present for the 24-72 h pulse-labelled group. Thermotolerance induction was maximal 24 h after the heat treatment and then declined during the next 24 h. The increased [3H]cholesterol/[3H]phospholipid ratio observed in response to hyperthermia resembles the processes that serve to provide homeoviscous adaptation to sustain thermosensitive membrane-located functional groups, in analogy with the mechanisms responsible for thermal adaptation. However, the lack of a positive correlation between thermotolerance induction and the changes in lipid synthesis, for the whole time interval studied, remains to be further explored before any mechanistic interpretation of the data can be found.

Acetates↗
PubMed1986

Relationship between cellular glutathione and hyperthermic toxicity in mammary carcinoma in mice.

This investigation evaluates in an in vivo system the possible correlation between the intracellular content of GSH and cysteine and thermal sensitivity and thermotolerance. The studies were performed on C3H mammary carcinomas, located on the hind paw of CBA mice. Intracellular thiols were measured by the HPLC technique and the degree of thermotolerance induction was determined from tumour growth rate studies. It was found that the intracellular GSH levels did not change significantly during thermotolerance induction, and that subtoxic hyperthermia induced a pronounced transient decrease in GSH down to 30 per cent of the control level. When the intracellular GSH level was decreased to the same extent, by pretreatment with D,L-buthionine-S-R-sulphoximine (BSO), thermotolerance was still inducible. Thus, the induction of heat-induced thermal resistance did not seem to be dependent on the intracellular GSH level. When hyperthermia and BSO were combined, the GSH levels were further reduced. Treatment with BSO slightly increased the toxicity of both thermotolerance-inducing and subtoxic hyperthermia. The cysteine concentrations increased several fold after BSO and heat treatments and contributed, under these conditions, to more than 25 per cent of the intracellular free reduced thiols. In general, there was no direct correlation between GSH and cysteine levels. It is concluded that thermotolerance induction does not depend on or cause changes in intracellular GSH levels and that subtoxic heat treatments induce a pronounced transient decrease in GSH concentration.

Animals↗
PubMed1983

Chemical reactivity and mutagenicity of some dihalomethanes.

Four dihalomethanes; dichloromethane, bromochloromethane, dibromomethane and diiodomethane, have been studied with respect to their reactivities towards nucleophilic compounds of different strengths in water solution and with respect to their toxicities and mutagenic effectiveness in bacterial test systems. The correlation between biological activity (toxicity and mutagenic effectiveness in Salmonella TA100) and reactivity towards strong nucleophiles indicates that reactions with nucleophilic groups of high reactivity in the biological material, possibly SH or amino groups in proteins, are involved in their mechanism of action.

Chemical Phenomena↗
PubMedDate not supplied

Increased antineoplastic activity of combined hyperthermic and bleomycin treatments in an adenocarcinoma after glutathione depletion in vivo.

We have earlier shown that glutathione depletion, achieved by BSO administration, only marginally increases the antineoplastic activity of hyperthermic or bleomycin treatments in C3H mammary adenocarcinoma, grown subcutaneously in the hind paw of CBA mice. In this study we evaluated the role of glutathione depletion on the antineoplastic activity of combined hyperthermic and bleomycin treatments on the same tumour model system. The activity was recorded by determination of tumour volumes 12 days after treatment and by tumour regression frequencies. When hyperthermic and bleomycin treatments were combined, their respective effects on the 12-day volume values were additive, irrespective of treatment sequence and presence of BSO. However, BSO increased significantly the tumour regression frequencies accomplished by combined hyperthermic and bleomycin treatments, particularly of hyperthermic treatments given together with or 24 h after bleomycin. It is not possible to conclude, at present, whether this effect is caused by low glutathione levels.

Adenocarcinoma↗