Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Endosomes were isolated from K 562 cells after 3 min after the endocytosis of a single cohort of transferrin molecules. 2. The change in 125I/59Fe ratio of heavy and light endosomes, relative to that of the transferrin used and 59Fe from light endosomes. 3. Incubation of heavy and light endosomes with PBS or PIH showed equal ATP specific iron release from both heavy and light endosomes, but in the presence of a NADH/NAD+ redox couple iron release from light endosomes was reduced. 4. Incubation of heavy and light endosomes with PIH and NEM did not completely abolish ATP specific iron release from heavy and light endosomes.
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PMID:Characteristics of iron release from isolated heavy and light endosomes. 316 66

This paper describes the distribution of NAD+-dependent 15-hydroxy prostaglandin dehydrogenase (delta13-reductase) in the mammalian brain and eye tissues. In addition, an NADH-dependent 15-ketoprostaglandin delta13-reductase (15-PGDH) activity was determined in the brain and eye tissue of some species. The rabbit brain and eye tissues were obtained after arterial perfusion with PBS buffer while the monkey, bovine and porcine tissues were obtained without any treatment. [3H]-PGF2alpha or [3H]-15-keto-17-phenyl-18,19,20-trinor-PGF2alpha1-1-isopropy l ester was incubated with different eye tissue preparations under various conditions. No 15-PGDH activity was observed in the monkey brain while 14% of exogenous PGF2alpha was metabolized to its 15-keto-13,14-dihydro-metabolite by the porcine brain. The 15-PGDH activity in the monkey eye tissue was undetectable. Both brain and different eye tissues hydrolysed 15-keto-17-phenyl-18,19,20-trinor-PGF2alpha-1-isopropyl ester to its free acid and the free acid was further metabolized to 15-keto-13,14-dihydro-17-phenyl-18,19,20-trinor-PGF2alpha by the reduction of 13,14-double bond indicating the presence of a delta13-reductase in these tissues. These data suggest that besides the presence of esterases the mammalian brain and eye tissues possess variable amounts of delta13-reductase in spite of their low 15-PGDH activity which may be of importance in physiology and drug metabolism of these tissues.
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PMID:Delta13-reductase dependent metabolism of prostaglandins in the mammalian brain and eye. 938 21

Indole-3-acetic acid (IAA) is toxic for human tumor cells and in association with horseradish peroxidase (HRP) can be used as a new prodrug/enzyme combination for targeted cancer therapy. The toxic effect of IAA on neutrophils, macrophages and lymphocytes is associated with cell peroxidase activity, which is high in neutrophils and low in lymphocytes. The effect of IAA on glucose and glutamine metabolism in leukocytes presenting different peroxidase activities: neutrophils, thioglycollate-elicited macrophages and lymphocytes was investigated. A time-course effect (from 6 to 48 h in culture) of IAA on glucose and glutamine metabolism of neutrophils, thioglycollate-elicited macrophages, and lymphocytes was then carried out. Addition of IAA (0.25 mM) did not have a marked effect on glucose utilization and lactate formation by the three cell types but it raised glutamine consumption and glutamate production by neutrophils and macrophages. IAA had no effect on glutamine consumption and glutamate production by lymphocytes. A strong relationship was found between glutamine utilization (0.999) and glutamate production (0.999) and peroxidase activity. IAA did not change the activities of hexokinase, glucose-6-phosphate dehydrogenase, citrate synthase, lactate dehydrogenase, and phosphate-dependent glutaminase of 24 h cultured neutrophils and lymphocytes. The effect of IAA (1 mM) on glucose and glutamine metabolism was also investigated by 1 h incubated leukocytes in PBS. IAA did not affect glucose and glutamine metabolism of lymphocytes but enhanced glucose and glutamine metabolism by 1 h incubated neutrophils and thioglycollate-elicited macrophages. IAA caused a marked increase on oxygen consumption by neutrophils, which was more pronounced in the presence of the glutamine as compared to glucose. The stimulation of oxygen consumption leads to a reduction in NADH/NAD+ ratio that activates the flux of substrates through the Krebs cycle. Since glutamine is mainly metabolized through the left hand side of the Krebs cycle, a reduction in the redox state of the cells may accelerate the flux of substrates through glutaminolysis. The toxic results presented here show that the affect of IAA in association with peroxidase involves activation of glutamine metabolism.
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PMID:Indole-3-acetic acid increases glutamine utilization by high peroxidase activity-presenting leukocytes. 1526 71

Male fertility and sperm quality are negatively impacted by obesity. Furthermore, recent evidence has shown that male offspring from obese rat mothers also have reduced sperm quality and fertility. Here, we extend work in this area by comparing the effects of both maternal obesity and offspring post-weaning diet-induced obesity, as well as their combination, on sperm quality in mice. We additionally tested whether administration of the NAD+-booster nicotinamide mononucleotide (NMN) can ameliorate the negative effects of obesity and maternal obesity on sperm quality. We previously showed that intraperitoneal (i.p.) injection of NMN can reduce the metabolic deficits induced by maternal obesity or post-weaning dietary obesity in mice. In this study, female mice were fed a high-fat diet (HFD) for 6 weeks until they were 18% heavier than a control diet group. Thereafter, HFD and control female mice were mated with control diet males, and male offspring were weaned into groups receiving control or HFD. At 30 weeks of age, mice received 500 mg/kg body weight NMN or vehicle PBS i.p. for 21 days. As expected, adiposity was increased by both maternal and post-weaning HFD but reduced by NMN supplementation. Post-weaning HFD reduced sperm count and motility, while maternal HFD increased offspring sperm DNA fragmentation and levels of aberrant sperm chromatin. There was no evidence that the combination of post-weaning and maternal HFD exacerbated the impacts in sperm quality suggesting that they impact spermatogenesis through different mechanisms. Surprisingly NMN reduced sperm count, vitality and increased sperm oxidative DNA damage, which was associated with increased NAD+ in testes. A subsequent experiment using oral NMN at 400 mg/kg body weight was not associated with reduced sperm viability, oxidative stress, mitochondrial dysfunction or increased NAD+ in testes, suggesting that the negative impacts on sperm could be dependent on dose or mode of administration.
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PMID:Impacts of obesity, maternal obesity and nicotinamide mononucleotide supplementation on sperm quality in mice. 3122 94