Tolerance of protein and lipid synthesis to mild hyperphenylalaninemia in developing rat brain

Geison, R. L.; Siegel, Frank L.

doi:10.1016/0006-8993(75)90327-3

Cited by 11 publications

(2 citation statements)

References 20 publications

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“…The inhibition of in uitro protein synthesis in brain tissue taken from hyperphenylalaninemic rats is about 50% (AOKI & SIEGEL, 1970). whereas only about 10% inhibition is found when protein synthesis is measured in uiuo (AGRAWAL et al, 1970;GEISON & SIEGEL, 1975). The reasons for this apparent discrepancy are not presently understood, and most research in this area has been directed toward gaining an understanding of the mechanisms producing the brain polyribosome disaggregation seen during hyperphenylalaninemia.…”

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confidence: 99%

EFFECTS OF ACUTE HYPERTHERMIA ON POLYRIBOSOMES, IN VIVO PROTEIN SYNTHESIS AND ORNITHINE DECARBOXYLASE ACTIVITY IN THE NEONATAL RAT BRAIN

Millan

Murdock

Bleier

et al. 1979

Journal of Neurochemistry

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Abstract— —Acute hyperthermia produces in situ disaggregation of brain polyribosomes in infant rats, as determined by electron microscopy. Protein synthesis is inhibited in infant, but not weanling, rat brain by 45 min of hyperthermia; this inhibition is reversed during a 2 h recovery period at normothermic conditions. Hepatic protein synthesis was inhibited less than that of brain. Acute hyperthermia also leads to a profound loss of ornithine decarboxylase activity in brain; during recovery the activity of this enzyme overshoots to values greater than those of normothermic control rats. This increase is blocked by cycloheximide administration. In testis, a tissue with high ornithine decarboxylase activity, enzyme activity was not affected by hyperthermia and recovery, indicating tissue specificity for these effects.

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confidence: 99%

EFFECTS OF ACUTE HYPERTHERMIA ON POLYRIBOSOMES, IN VIVO PROTEIN SYNTHESIS AND ORNITHINE DECARBOXYLASE ACTIVITY IN THE NEONATAL RAT BRAIN

Millan

Murdock

Bleier

et al. 1979

Journal of Neurochemistry

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“…While liver protein metabolism remains unaltered (Aoki & Siegel, 1970;Maclnnes & Schlesinger, 1971), acute hyperphenylalaninaemia causes a transient inhibition of brain protein synthesis (Aoki & Siegel, 1970;MacInnes & Schlesinger, 1971;Taub & Johnson, 1975;Hughes & Johnson, 1978), which appears to result from decreased rates of initiation (Taub & Johnson, 1975) and polypeptide-chain elongation (Hughes & Johnson, 1978). The loss of amino acids from the brain has been implicated by several investigators as the cause of the inhibition of brain protein synthesis during acute hyperphenylalaninaemia (Aoki & Siegel, 1970;Geison & Siegel, 1975;Hughes & P. Binek-Singerand T. C. Johnson Johnson, 1976;Berger et al, 1979). To provide further evidence for this hypothesis.…”

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The effects of chronic hyperphenylalaninaemia on mouse brain protein synthesis can be prevented by other amino acids

Binek-Singer¹,

Johnson²

1982

Biochemical Journal

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A prolonged elevation in the concentrations of circulating phenylalanine was maintained in newborn mice by daily injections of phenylalanine and a phenylalanine hydroxylase inhibitor, alpha-methylphenylalanine. The result of this chronic hyperphenylalaninaemia was an accumulation of vacant or inactive monoribosomes that persisted for 18 h of each day. An elongation assay in vitro with brain postmitochondrial supernatants demonstrated that, in addition, there was an equally prolonged decrease in the rates of polypeptide-chain elongation by the remaining brain polyribosomes. Analyses of the free amino acid composition in the brains of hyperphenylalaninaemic mice showed a loss of several amino acids from the brain, particularly the large, neutral amino acids, which are co- or counter-transported across plasma membranes with phenylalanine. When a mixture of these amino acids (leucine, isoleucine, valine, threonine, tryptophan, tyrosine, methionine) was injected into hyperphenylalaninaemic mice, there was an immediate cessation of monoribosome accumulation in the brain and there was no inhibition of the rates of polypeptide-chain elongation. Although the concentrations of the large, neutral amino acids in the brain were partially preserved by treatment of hyperphenylalaninaemic mice with the amino acid mixture, the elevated concentrations of phenylalanine remained unaltered. The amino acid mixture had no detectable effect on brain protein synthesis in the absence of the hyperphenylalaninaemic condition.

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Developmental Changes in Cerebral Amino Acids and Protein Metabolism

Lajtha

Sershen

Dunlop

1988

Amino Acid Availability and Brain Function in Health and Disease

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Tolerance of protein and lipid synthesis to mild hyperphenylalaninemia in developing rat brain

Cited by 11 publications

References 20 publications

EFFECTS OF ACUTE HYPERTHERMIA ON POLYRIBOSOMES, IN VIVO PROTEIN SYNTHESIS AND ORNITHINE DECARBOXYLASE ACTIVITY IN THE NEONATAL RAT BRAIN

EFFECTS OF ACUTE HYPERTHERMIA ON POLYRIBOSOMES, IN VIVO PROTEIN SYNTHESIS AND ORNITHINE DECARBOXYLASE ACTIVITY IN THE NEONATAL RAT BRAIN

The effects of chronic hyperphenylalaninaemia on mouse brain protein synthesis can be prevented by other amino acids

Developmental Changes in Cerebral Amino Acids and Protein Metabolism

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