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At least 1,783 records · Page 99Linked to original sources
PubMed2003

Use of the mannitol pathway in fructose fermentation of Oenococcus oeni due to limiting redox regeneration capacity of the ethanol pathway.

The heterolactic bacterium Oenococcus oeni ferments fructose by a mixed heterolactic/mannitol fermentation. For heterolactic fermentation of fructose, the phosphoketolase pathway is used. The excess NAD(P)H from the phosphoketolase pathway is reoxidized by fructose (yielding mannitol). It is shown here that, under conditions of C-limitation or decreased growth rates, fructose can be fermented by heterolactic fermentation yielding nearly stoichiometric amounts of lactate, ethanol and CO(2). Quantitative evaluation of NAD(P)H-producing (phosphoketolase pathway) and -reoxidizing (ethanol, mannitol and erythritol pathways) reactions demonstrated that at high growth rates or in batch cultures the ethanol pathway does not have sufficient capacity for NAD(P)H reoxidation, requiring additional use of the mannitol pathway to maintain the growth rate. In addition, insufficient capacities to reoxidize NAD(P)H causes inhibition of growth, whereas increased NAD(P)H reoxidation by electron acceptors such as pyruvate increases the growth rate.

Aldehyde-Lyases↗
PubMed1991

A case of the Rett syndrome with acute encephalopathy induced during calcium hopantenate treatment.

We report a girl with the Rett syndrome who had acute encephalopathy probably induced by calcium hopantenate (HOPA). This 4-year-6-month-old girl had a history of moderate developmental delay and had received HOPA administration when first admitted at 2 years 6 months of age with hypoglycemia, hyperammonemia, lactic and pyruvic acidemia, and non-ketotic dicarboxylic aciduria. After this episode, she showed the rapid destructive stage of the Rett syndrome, i.e., severe psychomotor retardation with loss of speech, peculiar stereotypic hand movements, autistic behavior and seizures. Despite subsequent investigations, including analysis of urinary metabolites of organic and amino acids, measurement of serum carnitine and a muscle biopsy, we could not clarify the primary metabolic abnormalities in this girl.

Acute Disease↗
PubMed1987

[Pharmacological studies on Y-8894 (VI). The effect on monoamine uptake and turnover in mouse brain].

The effect of Y-8894 (+/-) 2-[[o-(2-thenyl)phenoxy]methyl] morpholine maleate, which has been shown to improve experimentally induced learning and memory deficits, on cerebral monoamine uptake and turnover was studied in the mouse. The following results were obtained: 1) It inhibited in vitro norepinephrine (NE) uptake to the mouse cerebral synaptosomal fractions about 800 and 1250 times more potently than it did those of dopamine (DA) and serotonin (5-HT), respectively. 2) It dose-dependently inhibited in vivo NE uptake, but not DA or 5-HT uptake. 3) It reduced the accumulation of the NE metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), increased that of the 5-HT metabolite, 5-hydroxyindoleacetic acid (5-HIAA), and had no effect on that of the DA metabolite, homovanillic acid (HVA). These effects were compared with those of imipramine, calcium hopantenate (Ca-hopantenate) and dihydroergotoxine. Y-8894 appeared to act by stimulating the noradrenergic receptor, and it acts to a lesser extent by blocking the serotonergic receptor in the brain.

Animals↗