INT159946
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Temporal study of acetaminophen (APAP) and S-adenosyl-L-methionine (SAMe) effects on subcellular hepatic SAMe levels and methionine adenosyltransferase (MAT) expression and activity. | |||||||||||||||
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Studies further examined MAT expression and activity in response to APAP toxicity. | |||||||||||||||
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MAT expression was examined by Western blot. | |||||||||||||||
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In addition they measured the synthesis of AdoMet by adenosyl transferase and AdoMet utilization by COMT, and concluded that the decrease in AdoMet levels was a consequence of increased utilization during aging. | |||||||||||||||
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SAMe is synthesized in cells through the action of methionine adenosyltransferase (MAT). | |||||||||||||||
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It could be suggested that AdoMet levels in the brain tissue of the APP/PS1 mice, used in this study, do not decrease during aging because of less demand caused by neurodegeneration. | |||||||||||||||
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In addition they measured the synthesis of AdoMet by adenosyl transferase and AdoMet utilization by COMT, and concluded that the decrease in AdoMet levels was a consequence of increased utilization during aging. | |||||||||||||||
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The finding that AdoMet levels do not differ between the genotypes in (young) 8-month-old mice, but do differ in (older) 15-month-old APP/PS1 mice compared to their wild type littermates, suggests that alterations in AdoMet are a consequence of AD pathology rather than a cause, and it could be suggested that it is the result of neurodegeneration during aging (Fig. 2). | |||||||||||||||
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AdoMet and AdoHcy might also influence AD like pathology and vascular health [16] and it could be hypothesized that the above-mentioned nutritional components may influence and AdoMet and AdoHcy levels as well.
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AdoMet is a biological methyl donor and is a product of the conversion of methionine and ATP. | |||||||||||||||
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Stramentinoli et al. found decreased AdoMet levels in brain tissue of aging rats [33]. | |||||||||||||||
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This is the first study describing AdoMet and AdoHcy levels in brain tissue of aging mice. | |||||||||||||||
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However, because of a lack of brain tissue we only measured AdoMet and AdoHcy levels in this experiment. | |||||||||||||||
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For example, AdoMet administration in human neuroblastoma cells down regulates PS1 gene expression and A? | |||||||||||||||
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The finding that cholesterol- or DHA-containing diets do not alter AdoMet or AdoHcy levels in brain tissue of either wild type or APP/PS1 mice, but in contrast do have effects on AD pathology and cerebral hemodynamics [7, 15, 29], suggests that cholesterol- or DHA-containing diets do not influence cerebral hemodynamics or AD pathology via the methylation cycle. | |||||||||||||||
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Neither a cholesterol- nor a DHA-containing diet did alter AdoMet or AdoHcy levels in brain tissue of 8- and 15-month-old APP/PS1 and wild-type mice as compared to the standard diet (data not shown).
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The finding that AdoMet levels in APP/PS1 mice are not decreased during aging (in contrast to wild-type mice), is probably related to less demand due to neurodegeneration. | |||||||||||||||
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This could have explained the high-AdoMet levels; however, the AdoMet levels in the 8-month-old APP/PS1 mice in our study, should have been increased compared to 8-month-old wild types, and that was not the case. | |||||||||||||||
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In addition, we showed that cholesterol-containing, or DHA-enriched diets did not affect AdoMet or AdoHcy levels in brain tissue of APP/PS1 and wild-type mice. | |||||||||||||||
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This work was designed to see whether combination use of Gly and Mat could offer better liver protective and anti-hepatocarcinogenic effects than Gly or Mat alone, and whether it could reduce the adverse effects of Gly alone by acetaminophen-induced hepatotoxicity, diethylnitrosamine-induced hepatocarcinogenesis, induction of immunosuppression, albumen-induced swelling of rat hind paws. | |||||||||||||||
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