PubMed Health⌕ Search

Biomedical subjects

M Jägerstad

Publications and source records attributed to M Jägerstad.

At least 55 records · Page 3Linked to original sources
PubMed1985

Effects of meat composition and cooking conditions on the formation of mutagenic imidazoquinoxalines (MeIQx and its methyl derivatives).

In recent years it has been shown that certain methyl derivatives of 3H-imidazo[4,5-f]quinoxaline-2-amine are responsible for a major part of the mutagenicity formed during frying, broiling or baking of meat, and also formed in the preparation of meat extracts. The present study describes the precursors of these compounds and their formation with participation of Maillard or nonenzymatic browning reactions. The formation of these IQ-type mutagens was shown to occur when model systems of creatin(in)e, reducing monosaccharides, and certain amino acids were heated at 128 degrees C for 2 hr. In meat experiments, the mutagenicity was found to be significantly correlated with the presence of creatin(in)e in the meat samples. The same conditions that are favorable for Maillard reactions, such as supply of starting materials, high temperature, and a suitable water concentration, also increased the yield of mutagenicity during cooking. Fats seemed to act as regulators of the amount of heat transferred into the product rather than as reactants in the formation of mutagenicity.

Amino Acids↗
PubMed1984

Formation of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline in a model system by heating creatinine, glycine and glucose.

A mixture of creatinine, glucose and glycine was heated in diethylene glycol containing 14% water for 2 h at 128 degrees C, and the mutagens formed were purified by XAD-2 column chromatography, acid-base partition, Sephadex LH-20 column chromatography, 'blue cotton' treatment and HPLC. Two mutagenic substances were isolated by HPLC. The major mutagen was identified by its UV absorption and mass and NMR spectra as 2-amino-3,8- dimethylimidazo [4,5-f]quinoxaline, which was originally isolated from fried beef. This finding supported the idea that creatinine, amino acids and sugars present in meat are precursors in the formation of the mutagenic imidazoquinoxaline derivative.

Chemical Phenomena↗
PubMed1984

Mutagenicity of some synthetic quinolines and quinoxalines related to IQ, MeIQ or MeIQx in Ames test.

3-Methyl- and 3,4-dimethyl-3H-imidazo[4,5-f]quinoline, 3,8-dimethyl-3H-imidazo[4,5-f]quinoxaline, N6-methyl- and N6,7-dimethylquinoline-5,6-diamine, as well as N6,3-dimethylquinoxaline-5,6-diamine, have been synthesized. Only the first-mentioned compound was active in Ames test; the response was equal for Salmonella typhimurium TA98 and TA100, regardless of enzymatic activation (S9). However, its mutagenicity to TA98 + S9 was 300-1300 times smaller than the values reported for the related compounds, 3-methyl- and 3,4-dimethyl-3H-imidazo[4,5-f]quinolin-2-amine ('IQ' and 'MeIQ'), and for 3,8-dimethyl-3H-imidazo[4,5-f]quinoxalin-2-amine ('MeIQx'). Hence, the presence of the imidazole ring and the 2-amino group in the molecule seems to be important for the high mutagenicity of the latter compounds.

Animals↗
PubMed1984

A balance study of 14C-labelled 3H-imidazo[4,5-f]quinolin-2-amines (IQ and MeIQ) in rats.

The absorption and excretion of 14C-labelled 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ) were studied in rats of both sexes. The excretion was rapid and within 24 hr more than 90% of the radioactivity had left the rats. After 72 hr the faecal excretion of both compounds was approximately 45-65% and the corresponding excretion via the urine amounted to 37-49%. Only 1-2% was left in the carcasses and less than 0.2% was found in the expired air. About 70% of the IQ and 80% of the MeIQ was found in the bile fluid in a separate 24-hr study. The two compounds had different biliary excretion patterns and the mutagenicity of the bile correlated closely with the excretion of radioactivity.

Animals↗
PubMed1984

Nutrient intake and health status of lactovegetarians: chemical analyses of diets using the duplicate portion sampling technique.

Six middle-aged lactovegetarians (three men and three women) collected copies of four 24-h diets using the duplicate portion sampling technique. By chemical analyses, the nutrient composition of the lactovegetarian diet was determined in detail and compared with that of a mixed Swedish diet (normal) and a vegan diet (vegan) studied previously. The nutrient composition of the lactovegetarian diet expressed per 1000 kcal represented an average between normal and vegan diets. It was in closer agreement with Swedish recommended dietary allowances than the normal Swedish diet. Thus, the lactovegetarian diet contained 35% of the energy as fat and was rich in polyunsaturated fatty acids, especially linoleic acid, which resulted in a polyunsaturated/saturated fat ratio of 0.6. The lactovegetarian diet had a cholesterol concentration only half of that of a normal diet. Protein content and amino acid composition were well above recommendations. The lactovegetarian diets contained less sucrose than normal and vegan diets, but the sum of the intake of low molecular weight carbohydrates was comparable to normal and vegan diets. Dietary fiber was three times higher than in a normal diet. Essential minerals and trace elements, ie, Ca, Mg, Na, K, Fe, Zn, Cu, Se, satisfied current requirements. The intake of vitamin B12 by the lactovegetarians was around 1.4 micrograms daily, which is below the recommendations. The intake of folates was high, 300 to 400 micrograms daily. The clinical and biochemical investigation of the subjects revealed no signs of nutritional deficiency. Their plasma lipoproteins and the blood pressures were low for their age, in agreement with observations made earlier in a group of vegans.

Animals↗
PubMed1982

Effect of experimental folate deficiency on lipid metabolism in liver and brain.

1. Rats were given a purified folate-deficient diet containing 5 g succinylsulphathiazole/kg for 4-5 months in two experiments. Control rats were supplemented with folic acid in the drinking-water. 2. Weight gain was much below normal in the folate-deprived rats after the first month. Very low folate levels were recorded in blood, liver and peripheral nerve (12-33% of control). In the central nervous system, including the cerebrospinal fluid, the folate depletion was less conspicuous (50-80% of control). Only marginal signs of anaemia were found and no signs of neurological dysfunction were detected, using nerve conduction velocity measurement and co-ordination tests. 3. Light and electron microscopy of the folate deficient liver revealed fatty infiltration, and enlargement of liver parenchymal cells, nuclei and nucleoli. There was often a considerable amount of bile ductular cells in the lobuli but no cirrhosis. The morphological changes resembled those observed in choline deficiency. 4. Phospholipid N-methylation in liver was depressed in folate-deficiency. This was probably due to a decreased availability of S-adenosylmethionine caused by the low concentrations of methylated folate in liver. Intraperitoneal administration of methionine did not normalize phospholipid methylation. 5. In folate deficiency the proportion of ethanolamine phosphoglyceride in liver was increased at the expense of choline phosphoglyceride, which is consistent with a decreased phospholipid methylation. Also an increase in liver triacylglycerol was noted, in accordance with the morphological observations. Brain lipid composition was unchanged. 6. After the injection of labelled ethanolamine, isotope accumulated in liver phosphoethanolamine in folate deficiency, probably due to an impairment of the CTP:ethanolaminephosphate cytidylyltransferase (EC 2.7.7.14) reaction. The mechanism of this impairment is discussed. 7. Although the low concentrations of folate was the main nutritional change in the deprived animals, changes with respect to vitamin B12 and maybe also choline cannot be excluded. We conclude that some of the changes in folate deficiency, i.e. fatty liver and decreased biosynthesis of liver phospholipids may be due to a precipitated deficiency of lipotropic agents, whereas other differences may be specific for deficiency of folate per se, such as changes in liver phospholipid fatty acids and some of the morphological aberrations.

Animals↗
PubMed1981

Nutrient intake and health status of vegans. Chemical analyses of diets using the duplicate portion sampling technique.

A strict vegetarian diet [vegan diet (VD)] was investigated. Six middle-aged vegans (three men and three women) collected copies of 24-h diets using the duplicate portion sampling technique. By chemical analyses, the nutrient composition was determined in detail and compared with corresponding figures of a normal mixed Swedish diet. In the VD 30% of the energy originated from fat compared with 40% in normal Swedish mixed diet (MD). Linoleic acid was the dominant fatty acid (60% of total fat in VD versus 8% in MD). The VD contained 24 g protein/1000 kcal compared to 30 g/1000 kcal in MD, but the intake of essential amino acids by the vegans exceeded the recommendations. Dietary fiber was about 5 times higher in the vegan diet (29 versus 6 g/1000 kcal) and sucrose similar to MD (18 versus 21 g/1000 kcal). Among the inorganic nutrients the concentration of calcium (351 versus 391 mg/1000 kcal) and sodium (53 versus 49 mmol/1000 kcal) were similar in both types of diets but the amount of potassium (56 versus 30 mmol/1000 kcal, magnesium (300 versus 110 mg/1000 kcal), iron (9 versus 6.5 mg/1000 kcal), zinc (6.5 versus 4.7 mg/1000 kcal), and copper (2 versus 0.7 mg/1000 kcal) were nearly doubled. Iodine (39 versus 156 micrograms/1000 kcal and selenium (5 versus 17 micrograms/1000 kcal) were much lower in the VD, selenium even being undetectable in several 24-h diets. The VD was rich in folic acid (301 versus 90 micrograms/1000 kcal in MD) but the intake of vitamin B12 was only 0.3 to 0.4 microgram/day (MD: 3 to 4 micrograms/day). No clinical signs of nutritional deficiency were observed in the vegans. Serum protein levels of the vegans as well as their serum lipoproteins were near the lower range of the reference group. In addition, none of the vegans was overweight and their blood pressures were low for their age.

Blood Pressure↗
PubMed1980

Comparison of energy and nutrient intakes in women with high and low blood pressure levels.

The present study found no link between the intake of energy and various nutrients, on the one hand, and high or low blood pressure (BP) in women, on the other. Sixty women not on treatment for hypertension were selected from a defined population and examined, applying the duplicate portion technique, with respect to the relationships between BP and the intake of energy and nutrients. They were selected from above the 95th percentile for BP (group A) and from below the 30th (group B). The two groups were age-matched. The food sampling comprised six days, divided into three periods of two consecutive days within a period of four weeks. Twenty-four hour urine specimens were collected in each period and on two other occasions. The mean values for intake of energy, fat, protein, carbohydrates, minerals and electrolytes did not differ between the two groups despite the large differences in BP and obesity. The mean values for urinary excretion of minerals, electrolytes and nitrogen (calculated as crude protein) did not differ between groups. The present findings for the effect of salt on BP do not justify restriction of the salt intake as a means for decreasing BP in the population.

Adult↗
PubMed1979

Lipid composition and metabolism in liver and brain of vitamin B12-deficient rat sucklings.

1. Rat sucklings (18-d-old) bred from vitamin B12-deprived dams were compared with vitamin B12-supplemented dams' offspring, which were considered normal rat sucklings. 2. The vitamin B12-deficient rat sucklings had lower body-weight, liver weight and brain weight. 3. Vitamin B12 deficiency was also evident from the tenfold lower concentrations of vitamin B12 in liver and cerebellum. 4. The concentration of liver lipid was markedly increased in vitamin B12-deficient rats; triacylglycerol accounted for most of the increase. In brain the lipid concentration was slightly decreased (less than 0.05). 5. The methylation of ethanolamine phosphoglyceride to choline phosphoglyceride was reduced in both liver and brain in vitamin B12-deficient rats, as measured after the administration of [14C]ethanolamine. A slight decrease in choline phosphoglyceride concentration could be a consequence of this finding. The composition of phospholipids was otherwise normal. 6. Odd-chain fatty acids (pentadecanoate and heptadecanoate) accumulated in both liver and brain of the vitamin B12-deficient rat sucklings and constituted approximately 1% of total fatty acid. 7. The biosynthesis of fatty acid and cholesterol from intraperitoneally-injected 3H2O and [14C]propionate was unchanged in vitamin B12 deficiency.

Animals↗
PubMed1979

Pteroylpolyglutamate hydrolase of human granulocytes. I. Partial purification and kinetic studies.

Pteroylpolyglutamate hydrolase was demonstrated in the lysosome-like cytoplasmic granules of human granulocytes. Partial purification of this enzyme from granulocytes, obtained from patients with chronic myeloid leukaemia, was achieved by chromatography of the granule extract on Sephadex G-75, Bio-Rex 70 and hydroxylapatite. The enzyme preparation obtained was slightly contaminated with myeloperoxidase. Synthetic pteroyltetraglutamate was used as a substrate for the enzyme. The pH optimum was 5.1; the Km was 6 x 10(-3) mol/l; and the enzyme was activated by divalent cations, e.g. Ca++, Mg++ and Mn++. Pteroylpolyglutamate hydrolase is suggested to be involved in the destruction of microorganisms in granulocytes during phagocytosis.

Biological Assay↗
PubMed1979

The role of liver passage for conversion of pteroylmonoglutamate and pteroyltriglutamate to active folate coenzyme.

In an attempt to clarify the possible site of conversion of folates to active methylated coenzyme forms mono- and triglutamate was injected rapidly into the portal vein of dogs. Samples of blood were removed at various intervals from catheters placed in the portal vein, the hepatic vein and the femoral artery for assay carried out both with L. casei, S. Faecalis and liquid scintillating counting. Unreduced monoglutamates were extracted in the liver, immediately converted to methyltetrahydrofolate and released again to plasma from which it was slowly taken up by peripheral tissue. Reduced folates were refused by the liver. Triglutamates were extracted exclusively in the systemic circulation, converted to unreduced monoglutamate later to be reduced in the liver. No tissue displacement of folate was demonstrated. Only small amounts of monoglutamates, mainly reduced forms, were lost in the urine during the experiments. The kinetics of unreduced monoglutamate suggest a one compartment system, while the kinetics of methyltetrahydrofolate and triglutamate may implicate a two compartment system.

Animals↗
PubMed1978

Effects of vitamin B12 deficiency on lipid metabolism of the rat liver and nervous system.

1. Rats bred from vitamin B12-depleted dams were fed on a vitamin B12-deficient diet for 12-15 months and developed a severe vitamin B12 deficiency, as judged from methylmalonic acid excretion and tissue vitamin B12 levels at slaughter. Control rats were supplemented with vitamin B12 in the drinking-water. 2. Neurological signs were recorded after 7 months but the motor nerve conduction velocities remained normal. Neuropathological examination revealed mild changes in the peripheral nerves but no changes in the central nervous system. 3. The amounts of total lipids and phospholipids were normal, but in all examined tissues the proportions of pentadecanoate (C15 fatty acid) and heptadecanoate (C17 fatty acid) were considerably increased in vitamin B12 deficiency. 4. 3H2O was incorporated to the same extent into the fatty acids of nervous tissue from vitamin B12-deficient and control rats after 48 h. Less 3H was found in the liver fatty acids of the vitamin B12-deficient rats. 5. Neurological dysfunction can be demonstrated in the vitamin B12-deficient rat; the relation of the biochemical and neuropathological changes to the neurological signs needs further study.

Animals↗
PubMed1978

Effect of vitamin B12 deficiency on phosphatidylethanolamine methylation in rat liver.

1. In vitamin B12 deficiency the activity of tetrahydropteroylglutamate methyltransferase (EC 2.1.1.13) is depressed and the synthesis of methionine is reduced. Because the methyl group of methionine is largely utilized for the methylation of phosphatidylethanolamine, we investigated the effects of vitamin B12 deficiency on phosphatidylcholine synthesis. 2. The incorporation of injected [14C]formaldehyde into liver phosphatidylcholine was reduced by approximately 50% in vitamin B12-deficient rats. Also the corresponding incorporation of 5-[14C]methyltetrahydrofolic acid tended to decrease. The findings are consistent with a lower conversion of these precursors to methionine. 3. The effect of the deficient methyl-group supply on phosphatidylcholine synthesis was also investigated by the injection of [14C]ethanolamine. The amount (%) of lipid-14C recovered in phosphatidylcholine was significantly reduced in vitamin B12 deficiency. 4. Chemical analysis of liver phospholipids showed that the vitamin B12-deficient rats had a higher proportion of phosphatidylethanolamine and a lower proportion of phosphatidylcholine, indicating that the impaired synthesis of phosphatidylcholine by methylation leads to changes in membrane phospholipid composition.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1978

Lipid metabolism in the vitamin-B12-deprived rat.

Rats were deprived of vitamin B12 in order to study the effect of this deprivation on the metabolism of lipids in the liver and the nervous system. Serum vitamin B12 concentrations of 102.7 and 78 pg/ml were found at sacrifice after 5 and 6 months, respectively. Neurological testing failed to reveal signs of neuropathy. The total liver lipids were decreased in the vitamin-B12-deprived animals, but no changes were detected in the lipid concentration or in the phospholipid composition of the nervous system. Some animals were given propionate, and in these, contrary to expectations, pentadecanoic acid and heptadecanoic acid were found in smaller amounts in the liver triglycerides of the vitamin B12-deprived rats than in the control rats. This could be due to the inhibitory effect of methylmalonyl CoA on fatty-acid synthesis, demonstrated by others in vitro.

Animals↗
PubMed1978

Vitamin B12 deprivation in the rat: effects on folate metabolism with emphasis on the nervous system.

Rats were subjected to deprivation of vitamin B12 in order to induce neuropathy and to study effect on folate metabolism. Plasma vitamin B12 concentrations were maintained at about 100 pg/ml for 5 months. Neurological testing failed to reveal signs of neuropathy. Vitamin B12 deprivation induced high plasma folate levels but had no effects on the levels of total folate in the liver or the nervous system, probably because of an adequate methionine supply. If the rats were starved, a smaller proportion of 5-methyltetrahydrofolate was found both in liver and brain of the vitamin-B12-deprived animals. The folate concentration in the cerebrospinal fluid was lower than in the plasma but the values were correlated. There was a striking similarity between the liver and the brain in the way of handling 3H-folic acid and 14C-methyltetrahydrofolic acid. However, both substances showed a higher specific activity in the brain than in the liver, indicating a more dynamic state of brain folate.

Animals↗