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PubMedDate not supplied

S-adenosylmethionine or 5'-methylthioadenosine are unable to prevent fumonisin B1 hepatotoxicity in mice despite increased oxidation in liver.

Fumonisins are mycotoxins produced by the fugus Fusarium verticillioides, a common fungus growing on corn. Fumonisin B(1) (FB(1)) is the most toxic and prevalent fumonisin detected in corn and corn-based foods. It produces species-, gender-specific damage, and is hepatotoxic and nephrotoxic in rodents. Disruption of sphingolipid metabolism resulting from inhibition of ceramide synthase leads to alterations of cell signaling events, particularly tumor necrosis factor (TNF)alpha signal pathways and to the toxic effects of FB(1). It has been reported that FB(1) toxicity involves oxidative stress. S-adenosylmethionine (SAM) and methylthioadenosine (MTA), an intermediate metabolite in SAM metabolism, are hepatoprotective by modulating TNFalpha expression and increasing reduced glutathione (GSH) levels. The current study investigated the effects of SAM and MTA on FB(1) hepatotoxicity in C57BL/6N mice. The animals were given SAM or MTA by intraperitoneal injection of 25 mg kg(-1) body weight every 12 h when they received subcutaneous injection of 2.25 mg FB(1) kg(-1) body weight once daily for 5 days. The results showed that neither SAM nor MTA protected FB(1)-induced liver damage indicated by the increases in activities of plasma alanine aminotransferase and aspartate aminotransferase as well as the number of apoptotic hepatocytes. Both agents prevented an increase of free sphingosine but not sphinganine. Neither SAM nor MTA modified the FB(1)-induced expression of TNFalpha, interleukin (IL)-1alpha or IL-1 receptor antagonist. The decreased GSH in liver following FB(1) treatment was not protected by either agent. The data indicate that SAM and MTA are ineffective in protecting against FB(1) toxic effects.

Animals↗
PubMed1976

Substrate-attached serum and cell proteins in adhesion of mouse fibroblasts.

The effects of serum and coatings of substrate-attached material (SAM, which remains tightly adherent to the substrate after EGTA-mediated removal of cells) on the kinetics of attachment of DNA-radiolabeled BALB/c 3T3. SV40-transformed 3T3, and concanavalin A-selected revertant cells to glass coverlips were studied. The presence of serum in the medium of attaching cells had a marked effect on (1) the initial time lag before stable attachment of cells, (2) the maximum level of attached cells, (3) the stability of attachment, and (4) pseudopodial spread of the cell over the substrate. These serum effects could be mimicked by measuring attachment in medium without serum and with use of serum-preadsorbed or 3T3 SAM-coated coverslips. Enzymatic treatment of serumpreadsorbed substrates indicated that the factor(s) in serum which affects attachment is very trypsin-sensitive. Serum preadsorption of substrates stimulated attachment of SVT2 cells in medium with serum in a manner very similar to the effects of 3T3 SAM coating, while attachment of 3T3 SAM coating, while attachment of 3T3 or revertant cells was unaffected. Slab gel electrophoretic analysis (PAGE-SDS gels) identified eight major serum proteins by Coomassie blue staining (a) which bind to the substrate in the absence of cells and (b) which persist on the substrate after growth to confluence of 3T3 or SVT2 cells; this suggests that major breakdown or serum-adsorbed components does not occur during growth of normal or transformed cells. Seven radioactive SAM proteins were detected by autoradiography in 3T3 or SVT2 SAM electropherograms -- two of which are high molecular weight components which correspond to the glucosamine-radiolabeled hyaluronate proteoglycans observed previously; the remaining five are newly-identified proteins in SAM (one of these proteins appears to be actin). 3T3 and SVT2 cells have unique proportions of these seven components. The data are consistent with the idea that normal or virus-transformed cells do not attach directly to the culture substrate, but to specific classes of substrate-adsorbed serum proteins via deposition of specific classes of cell surface proteins and polysaccharides.

Actins↗
PubMed2006

Attachment of streptavidin to beta-cyclodextrin molecular printboards via orthogonal host-guest and protein-ligand interactions.

Streptavidin (SAv) is attached to beta-cyclodextrin (beta-CD) self-assembled monolayers (SAMs) via orthogonal host-guest and SAv-biotin interactions. The orthogonal linkers consist of a biotin functionality for binding to SAv and adamantyl functionalities for host-guest interactions at beta-CD SAMs. SAv complexed to excess monovalent linker in solution and then attached to a beta-CD SAM could be removed by rinsing with a 10 mM beta-CD solution. When SAv was attached to the beta-CD SAM via the divalent linker, it was impossible to remove SAv from the surface by the same rinsing procedure. This is interpreted by assuming that two SAv binding pockets are oriented towards the beta-CD SAM resulting in (labile) divalent and (stable) tetravalent beta-CD-adamantyl interactions for the mono- and divalent linkers, respectively. This was confirmed by experiments at varying beta-CD concentrations. When the [linker]/[SAv] ratio is reduced, a clear trend in the divalent-linker case is seen: the less linker the more protein could be removed from the surface. It is proven that the orthogonality of the binding motifs and the stability of the divalent linker at the beta-CD SAM allows the stepwise assembly of the complex at the beta-CD SAM by first adsorbing the linker, followed by SAv. This stepwise assembly allows the controlled heterofunctionalization of surface-immobilized SAv.

Adsorption↗
PubMed2001

L-dopa upregulates the expression and activities of methionine adenosyl transferase and catechol-O-methyltransferase.

High nonphysiological doses of l-dopa are administered to Parkinson's disease (PD) patients, to replenish the depleted dopamine (DA). A large portion of the administered L-dopa and the newly formed DA undergoes methylation by reacting with S-adenosyl-L-methionine (SAM). In the process SAM, as well as L-dopa and DA, is utilized and great demands are placed on the transmethylation system. In this study we investigated whether L-dopa increases the transmethylation process by inducing methionine adenosyl transferase (MAT), the enzyme that produces SAM, and catechol-O-methyl transferase (COMT), the enzyme that transfers the methyl group from SAM to L-dopa and DA. Swiss Webster mice were injected with L-dopa, four times/day, for 1 to 16 days. Brain DA, 3-O-methyldopa (3-OMD), SAM, S-adenosylhomocysteine (SAH), MAT, and COMT were measured following a 24-h withdrawal period. An increase of 264% of brain DA occurred at days 2 and 3 after which it tapered to about 164% of control. The brain level of 3-OMD increased to 870% of the control. SAM was increased by 44% after the sixth day and SAH level was about double after the second day. After day 3, MAT activity was increased by about 35%. Western blot analysis showed that MAT is more clearly characterized in 10% mercaptoethanol reducing buffer in which 31.5-, 38- (beta), and 48-kDa (alpha1/alpha2) subunits were distinctly revealed. The induction of the 38-kDa and, more prominently, the 48-kDa subunits of MAT and the potential transactivator proteins of MAT, c-Jun/AP-1, was evident by day 6. The 31.5-kDa subunit was downregulated. COMT was detected as 24.7-, 30-, and 47.5-kDa bands in the brain, consistent with the membrane-bound COMT I (MB-COMT) and the dimeric COMT II. The 24.7- and the 30-kDa MB-COMT bands were induced in the brain by day 6 and peaked on day 9. The highlight of the study is the fact that L-dopa induces the enzymes MAT and COMT. In addition, the downturn in brain DA after the sixth day coincides with the increase in SAM and the 48-kDa MAT protein. Thus, during PD treatment with L-dopa the induction of MAT and COMT is likely to occur and in turn increase the methylation and reduction of L-dopa and DA that may help cause the tolerance or the wearing-off effect developed to L-dopa.

Animals↗
PubMed1991

Functionally complex muscles of the cat hindlimb. I. Patterns of activation across sartorius.

The cat sartorius (SA) can be divided functionally into an anterior (SAa), knee extensor portion and a medial (SAm), knee flexor portion; it can be further subdivided anatomically by multiple nerve branches into parallel longitudinal columns that terminate in a distributed insertion at the knee with a continuous range of moment arms. Thus, SA may be controlled by a discrete number of motoneuron task groups reflecting a small number of central command signals or by a continuum of activation patterns associated with a continuum of moment arms. To resolve this question, the activation patterns across the width of the SA were recorded with an electrode array during three kinematically different movements--treadmill locomotion, scratching and paw shaking, in awake, unrestrained cats. Uniformity of activation along the longitudinal axis was also examined because individual muscle fibers do not extend the length of the SA. In addition, the cutaneous reflex responses were recorded throughout all regions of the SA during locomotion. Two fascial surface-patch arrays, each carrying 4-8 pairs of bipolar EMG electrodes, were sutured to the inner surface of the SA, one placed proximally and the other more distally. Each array sampled separate sites across the anterior to medial axis of SA. During locomotion, two basic EMG patterns were observed: the two burst-per-step-cycle pattern typical of SAa and the single burst pattern typical of SAm. There was an abrupt transition in the pattern of activation recorded in the two parts of SA during locomotion, and no continuum in the activation pattern was observed. Stimulation of both sural and saphenous cutaneous nerves during locomotion produced reflex responses that were uniformly distributed throughout SA, in contrast to the regional differences noted during unperturbed walking. Similarly, during scratching and paw shaking all parts of the SA were active simultaneously but with regional differences in EMG amplitude. The abrupt functional border between SAa and SAm coincided with the division of the SA into a knee flexor vs. a knee extensor. In all cases, the quantitative and qualitative differences in SAa and SAm EMGs were uniformly recorded throughout the entire extent of SAa or SAm; i.e., there was no segregation of activity within either SAa or SAm. Furthermore, the time course of EMG from each proximal recording site was nearly identical to the corresponding distal site, indicating no segregation of function along the longitudinal axis of SA. These results indicate that SAa and SAm constitute the smallest functional modules that can be recruited in SA.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Morphological study of the cataractous lens of the senescence accelerated mouse.

A murine model of accelerated aging, the senescence accelerated mouse (SAM), has been developed. There are three accelerated senescence-resistant (SAM-R) strains and eight senescence-prone (SAM-P) strains. The SAM-P strains have an earlier onset and more rapid advancement of senescence resulting from a significantly shorter lifespan compared with the SAM-R strains. Spontaneous cataracts have been found in some individuals of the SAM-P/9 strain. The SAM-P/1 strain, which was used in the present study, has such systemic senescent characteristics as senile amyloidosis and alopecia, but it was previously thought that cataract does not occur in this strain. However, we found cataractous changes in the lens of these animals at early stages of their life. The earliest change was the appearance of a ripple-mark body at about 3 months of age. The number of rippled rings increased with age. These changes later induced refractive distortion of retinal vessels. Whole-mount flat preparations of the epithelium showed that the number of cells was markedly decreased at the advanced stages of cataract. At the late stages of life the lens cortex became liquefied and developed into a mature cataract. Cataract formation in this strain may be related to reduced viability of the lens epithelium.

Aging↗
PubMed2000

Effect of S-adenosylmethionine on hepatic injury from sequential cold and warm ischemia.

We investigated whether S-adenosylmethionine (SAM) treatment improved ischemic injury using perfused rat liver after sequential periods of 24 h cold and 20 min re-warming ischemia. SAM (100 micromol/L) was added to University of Wisconsin (UW) solution and Ringers lactate solution. After cold and sequential warm ischemia, releases of lactate dehydrogenase (LDH) and purine nucleoside phosphorylase (PNP) markedly increased during reperfusion. The increase in PNP was significantly reduced by SAM treatment. While the concentration of reduced glutathione (GSH) in ischemic livers significantly decreased, the concentration of glutathione disulfide (GSSG) increased. This decrease in GSH and increase in GSSG were suppressed by SAM treatment. Lipid peroxidation was elevated in cold and warm ischemic and reperfused livers, but this elevation was also prevented by SAM treatment. Hepatic ATP levels were decreased in the ischemic and reperfused livers to 42% of the control levels. However, treatment with SAM resulted in significantly higher ATP levels and preserved the concentration of AMP in ischemic livers. Our findings suggest that SAM prevents oxidative stress and lipid peroxidation and helps preserve hepatic energy metabolism.

Adenosine Triphosphate↗
PubMed2005

Volumetric localization of epileptic activities in tuberous sclerosis using synthetic aperture magnetometry.

BACKGROUND: Magnetoencephalography (MEG) is a novel noninvasive technique for localizing epileptic zones. Tuberous sclerosis complex (TSC) is often associated with medically refractory epilepsy with multiple epileptic zones. Surgical treatment of TSC requires accurate localization of epileptogenic tubers. OBJECTIVE: The objective of this study was to introduce a new MEG technique, synthetic aperture magnetometry (SAM), to volumetrically localize irritable zones and clarify the correlations between SAM, dipole modeling and anatomical tubers. MATERIALS AND METHODS: Eight pediatric patients with TSC confirmed by clinical and neuroimaging findings were retrospectively studied. MEG data were recorded using a whole-cortex CTF OMEGA system. Sleep deprivation was employed to provoke epileptiform activity. Irritable zones were localized using both dipole modeling and SAM. RESULTS: MRI detected 42 tubers in the eight patients. Dipole modeling localized 28 irritable zones, and 19 out of the 28 zones were near tubers (19/42, 45%). SAM found 51 irritable zones, and 31 out of the 51 zones were near tubers (31/42, 74%). Among the 51 irritable zones determined by SAM, thirty-five zones were in 1-35 Hz, nine zones were in 35-60 Hz, and seven zones were in 60-120 Hz. CONCLUSIONS: The new method, SAM, yielded very plausible equivalent sources for patients who showed anatomical tubers on MRI. Compared to conventional dipole modeling, SAM appeared to offer increased detection of irritable zones and beneficial volumetric and frequency descriptions.

Brain Mapping↗
PubMed2006

Anisocotyly and meristem initiation in an unorthodox plant, Streptocarpus rexii (Gesneriaceae).

In common with most Old World Gesneriaceae; Streptocarpus Lindl. shows anisocotylous growth, i.e., the continuous growth of one cotyledon after germination. Linked to this phenomenon is an unorthodox behaviour of the shoot apical meristem (SAM) that determines the growth pattern of acaulescent species (subgenus Streptocarpus). In contrast caulescent species develop a conventional central post-embryonic SAM (mainly subgenus Streptocarpella). We used S. rexii Lindl. as a model to investigate anisocotyly and meristem initiation in Streptocarpus by using histological techniques and analyses of the expression pattern of the meristematic marker SrSTM1 during ontogeny. In contrast to Arabidopsis thaliana (L.) Heynh., S. rexii does not establish a SAM during embryogenesis, and the first evidence of a SAM-like structure occurs during post-embryonic development on the axis (the petiolode) between the two cotyledons. The expression pattern of SrSTM1 suggests a function in maintaining cell division activity in the cotyledons before becoming localized in the basal meristem, initially at the proximal ends of both cotyledons, later at the base of the continuously growing macrocotyledon, and the groove meristem on the petiolode. The latter is equivalent to a displaced SAM seemingly originating de novo under the influence of endogenous factors. Applied cytokinin retains SrSTM1expression in the small cotyledon, thus promoting isocotyly and re-establishment of a central post-embryonic SAM. Hormone-dependent delocalization of the process of meristem development could underlie anisocotyly and the unorthodox SAM formation in Streptocarpus.

Cotyledon↗
PubMed2006

Formation, maintenance and function of the shoot apical meristem in rice.

In higher plants, the process of embryogenesis establishes the plant body plan (body axes). On the basis of positional information specified by the body axes, the shoot apical meristem (SAM) and root apical meristem (RAM) differentiate at fixed positions early in embryogenesis. After germination, SAM and RAM are responsible for the development of the above-ground and below-ground parts, respectively, of the plant. Because of the importance of SAM function in plant development, the mechanisms of SAM formation during embryogenesis and of SAM maintenance and function in post-embryonic development are priority questions in plant developmental biology. Recent advances in molecular and genetic analysis of morphogenetic mutations in Arabidopsis have revealed several components required for SAM formation, maintenance and function. Although these processes are fundamental to the life cycle of every plant, conservation of the components does not explain the diversity of plant morphologies. Rice is used as a model plant of the grass family and of monocots because of the progress in research infrastructure, especially the collection of unique mutations and genome information. In comparison with the dicot Arabidopsis, rice has many unique organs or processes of development. This review summarizes what is known of the processes of SAM formation, maintenance and function in rice.

Genes, Plant↗
PubMed1989

Activation of rat liver S-adenosylmethionine decarboxylase by putrescine and 2-substituted 1,4-butanediamines.

1. The activation of S-adenosyl-L-methionine decarboxylase (SAM-DC) by putrescine and a series of 1,4-butanediamines with a substituent in position 2 was studied. 2. Kinetic data show the activation of SAM-DC by putrescine is essentially uncompetitive. 3. All 2-substituted 1,4-butanediamines were activators, although not as potent as putrescine itself. 4. At high concentrations of SAM activation of SAM-DC by putrescine and putrescine analogs deviated considerably from uncompetitive activation kinetics. 5. In order to explain the experimental data, especially the non-linearity of the "fractional velocity plots", it was necessary to postulate two independent, but equivalent activator binding sites, for which substrate (SAM) and activator compete. 6. Based on this kinetic model an equation was derived which describes the rate of SAM decarboxylation as a function of substrate and activator concentrations. 7. From the simulated curves, approximate values for equilibrium constants for the binding of activator and substrate to the activator binding sites, and relative rate constants for the product forming steps were calculated. 8. Even a minor change of the structure, such as the substitution of one hydrogen atom by fluorine in the 2-position of putrescine had a very considerable effect on the potency of activation. 9. It is apparent that the structural requirements of an activator of SAM-DC are highly specific.

Adenosylmethionine Decarboxylase↗
PubMed1984

Effects of hypophysectomy and immobilization stress on S-adenosylmethionine levels in rat adrenal glands.

Rat adrenal S-adenosylmethionine (SAM) levels and phenylethanolamine-N-methyltransferase (PNMT) activity were measured under conditions of hypophysectomy and stress. A new dual-label radioenzymatic assay for SAM is presented which eliminates problems found to exist with previous methods. Strain-specific differences in both PNMT and SAM were found, as well as sex differences in SAM levels. Immobilization stress resulted in an increase in adrenal SAM and PNMT activity, while hypophysectomy decreased both. The distribution of SAM between cortex and medulla did not change with either hypophysectomy or stress. Hypophysectomized Fisher rats were found to be capable of increasing PNMT activity in the absence of increased SAM levels.

Adrenal Glands↗
PubMed1995

Starvation-associated mutation in Escherichia coli strains defective in transcription repair coupling factor.

When E. coli WU3610 (tyrA14 ochre) bacteria are starved of tyrosine on the surface of glucose-salts agar plates, there is a progressive accumulation of slow growing prototrophic mutants that are neither revertants at the ochre codon nor any of the well characterised tRNA ochre suppressors. Isogenic derivatives defective in transcription repair coupling factor (mfd) showed normal starvation-associated mutation (SAM). WU361045, the original mfd strain, showed very much reduced SAM. At 37 degrees C this was associated with progressive loss of viability on plates but the defect in SAM was not due to loss of viability since incubation at 27 degrees C or addition of catalase prevented the loss of viability but did not restore SAM. Furthermore, mutants could not be rescued from starved WU361045 populations by a short period of tyrosine supplementation arguing that WU361045 was defective not in the survival of starvation-associated mutants, but in their formation. The SAM defect in WU361045 was not complemented by the katF gene on a low copy number plasmid. It is concluded that WU361045 carries an unidentified mutation, not under katF control, that greatly reduces SAM. If SAM is attributable to a spontaneously occurring DNA lesion, the latter is unlikely to be formed by hydrogen peroxide or active species derived from it.

Adaptation, Biological↗
PubMed1986

S-adenosyl-L-methionine and lead intoxication: its therapeutic effect varying the route of administration.

A comparative study on the effect of oral and subcutaneous (sc) or intravenous (iv) administration of S-adenosyl-L-methionine (SAM) in lead poisoning was carried out. SAM was given daily sc (20 mg/kg) and orally (80 mg/kg) to acute lead-intoxicated mice for 20 days. Chronic lead-poisoned patients received SAM, administered intravenously at a daily dose of 12 mg/kg or orally at a dose of 25-30 mg/kg. Independent of the method of administration in either animals or patients, GSH concentration in reduced lead intoxication was increased after SAM dosing. Corresponding blood lead content rapidly decreased and a significant recovery of hepatic and erythrocytic delta-aminolevulinate dehydratase (ALA-D), initially reduced, was clearly produced in the groups receiving SAM, although the response was slightly slower when SAM was given orally. It was found that the bulk of body lead burden was excreted in the feces, showing a peak within the first 24-48 hr and being much greater in animals treated with SAM. In these cases, urinary lead excretion was very low. Lead ALA-D inhibition was also evidenced by elevated urinary excretion of delta-aminolevulinic acid (ALA), porphobilinogen (PBG), and porphyrins. During treatment, precursors and porphyrins elimination declined, reaching normal levels soon after therapy ended. A good correlation between the recovery of both GSH levels and ALA-D activity and decreased lead content was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Ligand-binding characteristics of [3H]QNB, [3H]prazosin, [3H]rauwolscine, [3H]TCP and [3H]nitrendipine to cerebral cortical and hippocampal membranes of senescence accelerated mouse.

The senescence accelerated mouse (SAM) is known as a murine model of aging and memory dysfunction. In the cerebral cortical membranes of male 9-month-old SAM mice, the Bmax values of [3H]rauwolscine and [3H]nitrendipine binding, and the values of both Kd and Bmax of [3H]TCP binding in the accelerated aging strain SAM-P/8, were significantly increased compared with the values in the control strain SAM-R/1. In hippocampal membranes, however, the Bmax values of [3H]quinuclidinyl benzilate and [3H]nitrendipine binding were significantly decreased in SAM-P/8 compared with those in SAM-R/1. These results suggest that muscarinic acetylcholine receptors, alpha 2-adrenoceptors, N-methyl-D-aspartate receptor channels and L-type Ca2+ channels are changed in cerebral cortex and hippocampus in SAM-P/8 at 9 months.

Aging↗
PubMed1995

Age-related changes of mRNA expression of amyloid precursor protein in the brain of senescence-accelerated mouse.

APP695 mRNA is only expressed in the brains of SAM. The expression of APP mRNA in SAM P1 mice brains is more marked than that in SAM R1 mice brain. APP mRNA expression was increased with advancing age in all brain regions of SAM P1 mice compared with SAM R1. Especially, the changes of the amount of APP mRNA in the prosencephalon and the mesencephalon are significant at P value of 0.05. We suggest that overexpression of APP mRNA may be related to accelerated aging phenomenon in the SAM brain. This is the first report of age-related increase in the amount of APP mRNA in the SAM brain.

Aging↗
PubMed1992

Age-related changes in NMDA-induced [3H]acetylcholine release from brain slices of senescence-accelerated mouse.

From the brain slices of normal mice (ddY strain, subcloned from dd strain in National Institute of Health in Japan), N-methyl-D-aspartic acid (NMDA) at 0.01-1 mM evoked [3H]acetylcholine (ACh) release in a concentration dependent manner. [3H]ACh release evoked by 1 mM NMDA was significantly inhibited by 2-amino-5-phosphonovaleric acid (APV), phencyclidine (PCP) and 5-methyl-10,11-dihydroxy-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801). The effects of NMDA were not seen in the Ca2+ free medium and were inhibited by physiological concentration (0.83 mM) of Mg2+. NMDA seems to cause ACh release from nerve terminals through the receptor-ion channel mediated mechanism in the mouse brain. Based upon these results, we determined the activity of a high K(+)- or NMDA-evoked [3H]ACh release using prone/8 strain of senescence-accelerated mouse (SAM-P/8) (a murine model of accelerated aging and memory dysfunction) and SAM-resistance/1 strain (SAM-R/1) (normal aging mice as the control) and these release activities were compared between both strains and during aging. [3H]ACh release evoked by 30 mM KCl was significantly lower than that of age-matched SAM-R/1 at 9 and 12 months. NMDA evoked the [3H]ACh release at 2, 6, 10 and 14 months in R/1 mice. In SAM-P/8 mice the activity of NMDA-evoked release was seen at 2 months, but markedly decreased afterwards. Nonsignificant difference was observed on the uptake of [3H]choline and on the spontaneous release of [3H]ACh between SAM-P/8 and SAM-R/1 strains, and during aging.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMedDate not supplied

Betaine effects on hepatic methionine metabolism elicited by short-term ethanol feeding.

Previous studies in this laboratory have shown that feeding of ethanol to rats produces prompt inhibition of methionine synthetase (MS) as well as a subsequent increase in activity of betaine homocysteine methyltransferase (BHMT). Further studies have shown that supplemental dietary betaine enhanced methionine metabolism and S-adenosylmethionine (SAM) generation in control and ethanol-fed rats. Because MS and BHMT are both involved in the formation of SAM, this study was conducted to determine early effects of ethanol on hepatic SAM levels and the influence of betaine supplementation on parameters of methionine metabolism during the early periods of MS inhibition and enhanced BHMT activity. Results showed that ethanol feeding produced a significant loss in SAM in the first week with a return to normal SAM levels in the second week. Betaine feeding enhanced hepatic betaine pools in control as well as ethanol-fed animals. This feeding attenuated the early loss of SAM in ethanol-fed animals, produced an early increase in BHMT activity, and generated increased levels of SAM in both control and ethanol-fed groups. Furthermore, betaine lowered significantly the accumulation of hepatic triglyceride produced by ethanol after 2 weeks of ingestion.

Animals↗