Studies on the experimental phenylketonuria in rats.

Iijima, Satoshi; Ishii, Atsushi; Miyakoshi, Tatsuyoshi; Ōdaira, Tsunemoto; Musha, Morihiro

doi:10.1620/tjem.117.167

Cited by 4 publications

(1 citation statement)

References 10 publications

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“…Phenylpyruvate increased 4.21 fold ( p = 0.0098) in EOC only compared to normal but decreased −3.68 fold ( p = 0.036) in MOC compared to EOC. Phenyllactate (PLA) increased 195.45 fold ( p <0.0023) in EOC, a finding which is typically attributed to insufficient activity of phenylalanine hydroxylase [54]. Phenylacetate increased 1.93 fold ( p = 0.0203) in EOC compared to normal only, whereas 4-hydroxyphenylpyruvate was increased 17.82 fold ( p = 0.0069) in EOC compared to normal.…”

Section: Resultsmentioning

confidence: 97%

Identification of Metabolites in the Normal Ovary and Their Transformation in Primary and Metastatic Ovarian Cancer

2011

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In this study, we characterized the metabolome of the human ovary and identified metabolic alternations that coincide with primary epithelial ovarian cancer (EOC) and metastatic tumors resulting from primary ovarian cancer (MOC) using three analytical platforms: gas chromatography mass spectrometry (GC/MS) and liquid chromatography tandem mass spectrometry (LC/MS/MS) using buffer systems and instrument settings to catalog positive or negative ions. The human ovarian metabolome was found to contain 364 biochemicals and upon transformation of the ovary caused changes in energy utilization, altering metabolites associated with glycolysis and β-oxidation of fatty acids—such as carnitine (1.79 fold in EOC, p<0.001; 1.88 fold in MOC, p<0.001), acetylcarnitine (1.75 fold in EOC, p<0.001; 2.39 fold in MOC, p<0.001), and butyrylcarnitine (3.62 fold, p<0.0094 in EOC; 7.88 fold, p<0.001 in MOC). There were also significant changes in phenylalanine catabolism marked by increases in phenylpyruvate (4.21 fold; p = 0.0098) and phenyllactate (195.45 fold; p<0.0023) in EOC. Ovarian cancer also displayed an enhanced oxidative stress response as indicated by increases in 2-aminobutyrate in EOC (1.46 fold, p = 0.0316) and in MOC (2.25 fold, p<0.001) and several isoforms of tocopherols. We have also identified novel metabolites in the ovary, specifically N-acetylasparate and N-acetyl-aspartyl-glutamate, whose role in ovarian physiology has yet to be determined. These data enhance our understanding of the diverse biochemistry of the human ovary and demonstrate metabolic alterations upon transformation. Furthermore, metabolites with significant changes between groups provide insight into biochemical consequences of transformation and are candidate biomarkers of ovarian oncogenesis. Validation studies are warranted to determine whether these compounds have clinical utility in the diagnosis or clinical management of ovarian cancer patients.

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Section: Resultsmentioning

confidence: 97%

Identification of Metabolites in the Normal Ovary and Their Transformation in Primary and Metastatic Ovarian Cancer

2011

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Experimental hyperphenylalaninemia in the pregnant guinea pig: Possible phenylalanine teratogenesis and p‐chlorophenylalanine embryotoxicity

1987

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Maternal hyperphenylalaninemia (HPH) due to deficient phenylalanine (Phe) hydroxylation is a recognized human teratogen associated with an increased incidence of intrauterine growth retardation, microcephaly, congenital heart disease, and mental retardation. There are no previous reports of experimental HPH during organogenesis. Sustained HPH was produced in pregnant guinea pigs by adding 3.5% Phe and 1.0% parachlorophenylalanine (pCPA), an inhibitor of Phe hydroxylase, to standard guinea pig chow. Animals consumed the supplemented test diets from gestation day 1 until killed on gestation day 17. Examination of day 17 embryos revealed that embryonic mortality was associated only with maternal pCPA administration and was independent of the degree of maternal HPH. Embryonic malformation was associated with maternal HPH as well as maternal pCPA administration. Both maternal HPH and pCPA administration were associated with embryonic growth retardation. There was no association between maternal food intake or plasma tyrosine levels and embryonic abnormality or mortality. Both Phe and tyrosine were found to be concentrated in gestation day 17 yolk sac fluid when compared to maternal plasma Phe and tyrosine. The association of embryonic malformation and maternal HPH is consistent with human data. The embryotoxicity of pCPA requires further study and highlights the necessity of appropriate controls in models of experimental HPH.

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A new experimental model of hyperphenylalaninemia in rat. Effect of p-chlorophenylalanine and cotrimoxazole

et al. 1977

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Studies on the experimental phenylketonuria in rats.

Cited by 4 publications

References 10 publications

Identification of Metabolites in the Normal Ovary and Their Transformation in Primary and Metastatic Ovarian Cancer

Identification of Metabolites in the Normal Ovary and Their Transformation in Primary and Metastatic Ovarian Cancer

Experimental hyperphenylalaninemia in the pregnant guinea pig: Possible phenylalanine teratogenesis and p‐chlorophenylalanine embryotoxicity

A new experimental model of hyperphenylalaninemia in rat. Effect of p-chlorophenylalanine and cotrimoxazole

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