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PubMed1998

Lipotrope deficiency inhibits cell growth and induces programmed cell death in human breast cancer cell line MCF-7.

To determine the effects of lipotrope modification on breast cancer cell growth and cell death, the human breast cancer cell line MCF-7 was assigned to grow in one of three lipotrope treatment media for four days. The treatment media included lipotrope-control medium (LCM), containing all required lipotropes; lipotrope-deficient medium (LDM), lacking all lipotropes but supplying homocysteine instead; and lipotrope-additive medium (LAM), containing twice as much of each lipotrope as LCM. Cell count and [3H]thymidine incorporation into DNA revealed that LDM slowed cell growth and inhibited cell proliferation in the MCF-7 cell line. Gel electrophoresis showed significant DNA degradation with the appearance of fragments in LDM-treated cells, whereas the DNA in LCM and LAM cells was largely intact. The LDM group displayed more apoptotic bodies as detected by in situ immunohistochemistry. The gene expression level of bcl-2 was lower in cells treated with LDM than in those treated with LCM and LAM, whereas p53 gene expression did not appear different among the three treatment groups. It is concluded that lipotrope deficiency inhibits cell growth and induces programmed cell death in the human breast cancer cell line MCF-7.

Amino Acids↗
PubMed2004

Elevated erythrocyte CDP-choline levels associated with beta-thalassaemia in patients with transfusion independent anaemia.

The accumulation of CDP-ethanolamine as well as CDP-choline in a small cohort of patients with normal UMPH1 and no defined cause for their anaemia suggested a defect in both phosphotransferases. Here we report 10 patients with transfusion independent beta-thalassaemia; 8 being pure heterozygotes and 2 heterozygotes also for Hb E. Mean CDP-choline (86.xxx +/- 48 microM) and CDP-ethanolamine (34.6 microM +/- 34.5 microM), mean control <3 microM. Elevated CDP-choline in patients with no defined cause for their haemolytic anaemia was previously suggested as a possible indicator of CDP-choline phosphotransferase deficiency. Here we associate it with transfusion independent beta-thalassaemia.

Anemia↗
PubMed1983

Tissue distribution of methylcobalamin in rats fed amino acid-defined, methyl-deficient diets.

Total cobalamin and methylcobalamin levels were determined in tissues of male F344 rats fed a complete, amino acid-defined diet or a diet deficient in methionine, choline and/or cyanocobalamin. Total cobalamin levels in rats fed the complete diet were (picograms/milligram tissue +/- SEM): liver, 67 +/- 13; kidneys, 738 +/- 133; spleen, 23 +/- 2; and adrenals, 268 +/- 36. Corresponding methylcobalamin levels were: liver, 1.6 +/- 0.5; kidneys, 107.6 +/- 22.2; spleen, 0.3 +/- 0.1; and adrenals, 26.9 +/- 5.3; these values represent 2.4, 14.5, 1.4 and 9.7%, respectively, of the total cobalamin levels. Total cobalamin levels of all tissues studied were altered by cobalamin deprivation alone or in conjunction with methionine and/or choline deprivation. Methylcobalamin levels were more resistant to dietary alteration. Regardless of the presence or absence of methionine and cobalamin in the diet, choline deprivation always decreased the proportion of methylcobalamin in the liver. Kidney levels of methylcobalamin, like those of total cobalamin, were decreased by removal of cobalamin from the complete or the methyl-deficient diets. The results demonstrate that cobalamin, methionine and choline exert quite different effects on tissue levels of the cobalamins in rats.

Adrenal Glands↗
PubMed1992

Alzheimer's disease: a 'cobalaminergic' hypothesis.

An association between Alzheimer's Disease (AD) and low CSF and serum vitamin B12 (B12) has recently been described (1, 2, 3). This is apparently independent of nutritional intake (4). It has been suggested that such patients may exhibit an atypical form of cobalamin deficiency (3, 4). It is therefore proposed that these deficiencies may be aetiologically important, at least in sub-groups of AD, and a mechanism is described whereby B12 deficiency may result in the characteristic neurotransmitter changes of the disease. The hypothesis generates predictions regarding biochemical evaluation of such patients and suggests associations between the neurochemical disturbances and structural abnormalities of AD.

Alzheimer Disease↗
PubMed1988

Comparison of methyltransferase activities of pair-fed rats given adequate or methyl-deficient diets.

The short-term effects of a lipotrope-deficient (methyl-deficient) diet on tRNA and protein methyltransferase activities have been studied using pair-fed male Fischer rats. The activity of liver N2-guanine tRNA methyltransferase II (NMG2) of animals receiving the methyl-deficient diet (MDD) for 2 weeks was found to be elevated more than 2-fold. This is in agreement with the results of earlier experiments in which the animals were fed ad libitum. These data indicate that the effects of lipotrope-deficient diets on NMG2 activity observed in the earlier studies can be attributed to the nature of the diet, and not to differences in caloric intake. In the same pair-fed animals, very little effect of MDD on the activity of NMG2 of either brain or spleen was observed. In liver, the activity of one of the enzymes that catalyze protein methylation--protein methylase I (S-adenosyl-methionine: protein-arginine N-methyltransferase)--was significantly elevated in response to the lipotrope-deficient diet. In contrast, the activities of protein methylase II (S-adenosylmethionine: protein-carboxy-O-methyltransferase), from control and experimental animals did not differ significantly. Lipotrope-deficient diets are thus seen to induce, within a short period of time, selective changes in the activities of some, but not all, of the liver enzymes that catalyze the methylation of tRNA and protein.

Animals↗
PubMed2000

Interactive effects of methyl-deficiency and dietary restriction on liver cell proliferation and telomerase activity in Fischer 344 rats pretreated with aflatoxin B(1).

The effects of methyl-deficiency and dietary restriction (DR) on hepatic cell proliferation and telomerase activity was studied in male Fischer 344 rats pretreated with aflatoxin B(1) (AFB(1)). Five-week-old rats were gavaged 5 days per week for 3 weeks with AFB(1) (25 microg/rat per day) or solvent (100 microl 75% dimethylsulfoxide). Rats were then divided into four groups. Two groups were fed a methyl-sufficient (MS) diet either ab libitum (AL) or with DR. The other two groups were fed a methyl-deficient (MD) diet either AL or with DR. At 15, 20, and 32 weeks of age, hepatic cell proliferation, telomerase activity, and the number of glutathione S-transferase-P positive (GST-P(+)) foci were determined. DR reduced hepatic cell proliferation, while the MD diet and AFB(1) pretreatment increased cell proliferation. Telomerase activity was decreased by DR and increased by the MD diet and AFB(1) pretreatment. The same trend was observed with GST-P(+) foci: in AFB(1)-pretreated rats, methyl deficiency increased the number of foci, while DR decreased the number. These results are consistent with a role of telomerase in hepatocarcinogenesis.

Aflatoxin B1↗
PubMed1983

The temporal lobe in dementia of Alzheimer's type.

Evidence is presented of a predilection of neurofibrillary tangle formation and choline acetyltransferase deficiency for the temporal lobe in Alzheimer's disease. Together with evidence from studies of cerebral atrophy, 5-HT levels, and clinical findings, this indicates that changes in the temporal lobe may play a prominent role in Alzheimer's disease, especially in elderly patients.

Aged↗
PubMed1984

Hypomethylation of hepatic nuclear DNA in rats fed with a carcinogenic methyl-deficient diet.

A progressive decrease was observed in the 5-methyldeoxycytidine content of hepatic DNA in male F344 rats fed with a hepatocarcinogenic methyl-deficient diet. The same dietary regimen resulted in altered hepatic contents of S-adenosylmethionine, the methyl-donating species, and S-adenosylhomocysteine, an inhibitor of DNA methylase. The data indicate that this carcinogenic dietary manipulation is sufficient to alter a possible regulatory process, DNA methylation.

Animals↗
PubMed1986

Hepatocyte-like cells within the pancreas of rats fed methyl-deficient diets.

Administration of a methyl-group-deficient diet with or without an initial single injection of diethylnitrosamine to male Fischer 344 rats resulted in the development of cells structurally similar to hepatocytes that lay in small clusters around one or more islets of Langerhans in the pancreas. These cells were detected in 15/256 rats fed various methyl-deficient diets in study 1 and in 7/28 rats fed a severely methyl-group-deficient diet in study 2. The results of special staining procedures for the detection of glycogen, albumin and particulate iron uptake indicated that at least some of these cells shared features common to liver cells. These results, as well as previously reported observations of similar cells in hamsters treated with ethionine, provide additional evidence that the lack of available physiological methyl donors contributes to altered differentiation of pancreatic acinar cells.

Animals↗
PubMed1996

The AF64A model of cholinergic hypofunction: an update.

Based on numerous reports in the literature since 1980, one can now conclude that ethylcholine aziridinium (AF64A) is selective for the cholinergic system in vivo, and that the effect is both dose- and site-dependent. Thus, AF64A treatment, under the correct conditions of dose and time will result in selective reductions in levels of ACh, AChE, ChAT, HAChT, and K(+)- and ouabain-stimulated release of ACh. While other neurotransmitters may also be affected in brains of AF64A treated rats, the effect is only transient and is most probably secondary to the initial cholinergic deficit-induced by AF64A, reflecting an adaptive reaction of these neurotransmitter systems, which are normally integrated with cholinergic interconnections, to the cholinergic deficiency induced by AF64A. This paper provides a historical perspective for the development of AF64A as a selective cholinotoxin, and surveys its potential mechanisms of action at the neurochemical and molecular levels. Moreover, the availability of an animal model such as the AF64A-treated rat, in which the cholinergic system has been compromised selectively for an extended period of time, has allowed investigators to study a wide variety of questions that relate to factors controlling cholinergic function in vivo. Several key illustrations are presented at the end of this paper.

Animals↗
PubMed1988

Effects of unilateral ureteric occlusion on renal necrosis occurring in rats fed a methyl-deficient diet.

Wistar male rats were fed from weaning a methyl-deficient diet (groups I and II) or a standard commercial diet (groups III and IV). At the day 3 the left ureter was tied and divided in animals of groups I and III, while those in groups II and IV were sham operated. Rats of all groups were killed on days 8 and 10 to evaluate the incidence and extent of tubular necrosis (day 8) and tubular and cortical necrosis (day 10). The results of this study show that unilateral ureteric obstruction diminishes the incidence, severity and extent of necrosis in the same kidney.

Acute Kidney Injury↗
PubMed1995

Protective effect of coconut oil on renal necrosis occurring in rats fed a methyl-deficient diet.

Weanling rats fed a methyl-deficient diet develop renal necrosis with acute renal failure. The aim of this experiment was to explore further the role of coconut oil in this experimental model. Weanling Wistar male rats were fed methyl-deficient and their controls were fed methyl-supplemented diets. Coconut oil was fed at 14% and 20%, the latter concentration with and without 1% safflower oil (rich in linoleic acid); other groups received similar diets but instead of coconut oil, a mixture of hydrogenated vegetable oil and corn oil (rich in unsaturated fatty acids) was employed. Coconut oil fed at a 14% concentration did not evidence any protective outcome in relation to the renal lesions. Coconut oil at a 20% concentration showed a protective effect, mainly when the diet included safflower oil. The renal protective effect was evidenced by less or no mortality and increased survival time in the methyl-deficient rats receiving coconut oil, as well as by a reduced incidence (%) and severity of the renal lesions as evaluated by renal weight, and type (tubular and cortical necrosis or repair) and extent (grade) of the renal damage. The lack of a protective outcome when coconut oil was fed at 14%, along with the fact that in those rats receiving coconut oil at 20% the protection was greater when the diet was supplemented with 1% safflower oil, indicates that the protective effect should be attributed to the type of fatty acids coconut oil has and not to their shortage of essential fatty acids.

Animals↗
PubMed1999

alpha2-macroglobulin- and murinoglobulin-1- deficient mice. A mouse model for acute pancreatitis.

Mice deficient in either or both mouse alpha2-macroglobulin (MAM) and murinoglobulin-1 (MUG1) were generated and proved phenotypically normal under standard conditions. Acute pancreatitis was induced with a diet deficient in choline and methionine, supplemented with ethionine. The mortality was less than 25% in wild-type mice, as opposed to at least 56% in knockout mice, and was highest (70%) in MAM-/- mice, with earliest onset at 2 days. Plasma amylase and lipase levels were increased, but pancreatic tissue appeared histologically variable in individual mice. The clinical symptoms were most severe in MAM-/- mice and, surprisingly, were not aggravated in the double knockout mice, suggesting that the lack of proteinase inhibition capacity was not the major problem. Therefore, we analyzed the expression of 21 different cytokines and polypeptide factors in the pancreas of all experimental groups of mice. Interleukin-1-receptor antagonist mRNA was consistently induced by the diet in the pancreas of MAM-/- mice, and transforming growth factor-beta, tumor necrosis factor-alpha, tumor necrosis factor-beta, beta-lymphotoxin, and interferon-gamma mRNA levels were also increased. The data demonstrate the important role of alpha2-macroglobulin (A2M) in acute pancreatitis as both a proteinase inhibitor and a cytokine carrier. Mice deficient in MAM and/or MUG thus offer new experimental models for defining in vivo the role of the macroglobulins in pancreatitis and in other normal and pathological processes.

Acute Disease↗
PubMed1989

Altered expression of retrovirus-like sequences and cellular oncogenes in mice fed methyl-deficient diets.

Methyl-deficient (lipotrope-deficient) diets enhance liver carcinogenesis in rodents. Although the mechanisms responsible for the cancer-promoting activity of such diets have not been identified, they have been observed to cause impaired immune response, alterations in methylation of liver RNA and DNA, and enhanced susceptibility to oxidative damage. Since alterations in gene expression may also play a critical role, the present studies examined the expression of the c-myc, c-H-ras, epidermal growth factor receptor, and ornithine decarboxylase genes, as well as endogenous retrovirus-like sequences, in C57BL/6J x C3H/HeJ F1 mouse liver during the first 2 weeks of feeding of a methyl-deficient diet. The kinetics of liver cell proliferation was investigated in parallel. Increased [3H]thymidine incorporation into liver DNA was found at day 4 and reached a maximum at days 7-11 after commencement of the methyl-deficient diet, when compared to age-matched mice fed a complete diet. Northern blot analysis of polyadenylated liver RNA samples indicated an increase in the levels of RNA homologous to Moloney murine leukemia virus and intracisternal A particle sequences but no significant change in the level of VL30 retrovirus-related RNA in the samples from mice fed methyl-deficient diets. A marked increase in the levels of c-myc and a slight increase in the levels of ornithine decarboxylase and c-H-ras transcripts were seen in the liver RNA samples from the treated mice. Of particular interest was a decrease in the abundance of epidermal growth factor receptor transcripts in the liver RNA samples from the treated mice. These changes in cellular levels of specific RNA resemble, in several respects, those we have previously described in rodent liver during regeneration and tumor promotion and also those seen in rodent hepatomas. They may reflect, therefore, a common profile of gene expression relevant to cell proliferation.

Animals↗
PubMedDate not supplied

Alcohol-nutrition interaction: 1984 update.

Alcohol remains a prevailing cause of malnutrition resulting in a variety of deficiency states secondary to decreased intake of nutrients. In addition to various well described primary malnutrition syndromes, secondary malnutrition may result from the interaction of ethanol with nutrient digestion, absorption or utilization. Some of the latter alcohol-nutrient interactions have been recently defined and their pathogenesis is discussed in this review. Included are interactions with thiamine, folic acid, vitamin A and disorders secondary to amino acid imbalances. The rationale for various forms of therapy is reviewed, including the treatment aimed at correcting the "hypermetabolic state" in alcoholics ad the pitfalls of excess nutrient administration (particularly as it pertains to pyridoxine, vitamin A and amino acids). The desirability of recognizing early precirrhotic stages of alcoholic fibrosis is emphasized, in order to start therapy prior to the medical and/or social disintegration of the alcoholic.

Alcoholism↗
PubMed1990

L-azaserine induced preneoplasia in the rat pancreas. A morphometric study of dietary manipulation (lipotrope deficiency) and ultrastructural differentiation.

Putatively preneoplastic, pancreatic atypical acinar cell foci (AACF) and nodules (AACN), collectively termed atypical acinar cell lesions (AACL), were induced in male Lewis rats by L-azaserine (300 mg/kg body weight [bw] in divided doses). Rats given carcinogen and then fed a lipotrope deficient (LD) diet developed a significantly greater number of larger lesions than animals fed complete diet throughout the experiment. It is suggested that lipotrope deficiency plays a promoting role in this model of pancreatocarcinogenesis. Ultrastructural morphometric studies of AACF, when compared to control tissues, revealed the following significant results: 1) a decrease in surface area of cell cytoplasm with no change in nuclear area, and hence increased nucleus/cytoplasm (N/C) ratio; 2) a reduction in size and uniformity of zymogen granules; and 3) an increase in number of granules per microns 2 of cell. The results suggest that arrested development of the AACF cells is associated with reduced cytoplasm and zymogen production per cell. AACL may be eosinophilic due to an overall increased concentration of zymogen in these hyperplastic lesions and not because individual acinar cells in the AACL contain an increased amount of zymogen or are "zymogen-rich," as has been reported.

Animals↗