Altered Metabolism in a Streptococcus lactis C2 Mutant Deficient in Lactic Dehydrogenase

Streptococcus lactis UN possessed galactokinase, uridine diphosphate glucose epimerase (galacto-waldenase), hexokinase, aldolase, lactic dehydrogenase, alcohol dehydrogenase, and aldehyde dehydrogenase enzyme systems. The presence of galactokinase, galactowaldenase, and hexokinase indicated that monosaccharides, galactose, and glucose were phosphorylated and converted into glucose-6-phosphate, which then enters the glycolytic cycle. Galactokinase and UDPG epimerase enzymes were found to be adaptive in nature. However, hexokinase, aldolase, and dehydrogenases for lactate, alcohol, and aldehyde were found to be constitutive in nature, as the organism, regardless of the substrate used, always possessed these five enzymes. Both alcohol and aldehyde dehydrogenases were NAD-specific rather than NADP-specific.Penicillin, streptomycin, aureomycin, and terramycin inhibited the activities of these enzyme systems to varying degrees. Also, penicillin and streptomycin inhibited the production of galactokinase and UDPG epimerase by the organism, but had no effect upon the production of hexokinase.

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The isoenzymes of lactic dehydrogenase. II. Pulmonary embolism, liver disease, the postoperative state, and other medical conditions

Archives of Internal Medicine ◽

10.1001/archinte.119.4.333 ◽

1967 ◽

Vol 119 (4) ◽

pp. 333-344 ◽

Cited By ~ 3

Author(s):

N. P. Trujillo

Keyword(s):

Pulmonary Embolism ◽

Liver Disease ◽

Lactic Dehydrogenase ◽

Medical Conditions ◽

Postoperative State

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Renal infarction. Elevation of serum and urinary lactic dehydrogenase (LDH)

Archives of Internal Medicine ◽

10.1001/archinte.121.1.87 ◽

1968 ◽

Vol 121 (1) ◽

pp. 87-90 ◽

Cited By ~ 5

Author(s):

I. L. London

Keyword(s):

Lactic Dehydrogenase ◽

Renal Infarction

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Nomenclature Abstract for Streptococcus lactis lactis (Lister 1873) Garvie and Farrow 1982.

The NamesforLife Abstracts ◽

10.1601/nm.5654 ◽

2003 ◽

Author(s):

Charles Thomas Parker ◽

Nicole Danielle Osier ◽

George M Garrity

Keyword(s):

Streptococcus Lactis

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Lactic dehydrogenase isoenzyme

Japanese Journal of Oral Biology ◽

10.2330/joralbiosci1965.12.293 ◽

1970 ◽

Vol 12 (4) ◽

pp. 293-306

Author(s):

K. SUZUKI

Keyword(s):

Lactic Dehydrogenase ◽

Dehydrogenase Isoenzyme ◽

Lactic Dehydrogenase Isoenzyme

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Irisin Ameliorates Hypoxia/Reoxygenation-Induced Inflammation and Apoptosis in PC12 Cells by Inhibiting TLR4/MYD88 Signaling Pathway

Current Topics in Nutraceutical Research ◽

10.37290/ctnr2641-452x.17:329-336 ◽

2019 ◽

Vol 17 (3) ◽

pp. 329-336

Author(s):

Wang Jinli ◽

Xu Fenfen ◽

Zheng Yuan ◽

Cheng Xu ◽

Zhang Piaopiao ◽

...

Keyword(s):

Ischemic Stroke ◽

Signaling Pathway ◽

Pc12 Cells ◽

Major Complication ◽

Lactic Dehydrogenase ◽

Dependent Manner ◽

Cerebral Ischemic Stroke ◽

Cerebral Ischemic ◽

Myd88 Signaling ◽

Hypoxia Reoxygenation

Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.

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A multifactorial analysis of prognostic factors in patients with liver metastases from colorectal carcinoma.

Journal of Clinical Oncology ◽

10.1200/jco.1983.1.11.720 ◽

1983 ◽

Vol 1 (11) ◽

pp. 720-726 ◽

Cited By ~ 86

Author(s):

C J Lahr ◽

S J Soong ◽

G Cloud ◽

J W Smith ◽

M M Urist ◽

...

Keyword(s):

Alkaline Phosphatase ◽

Colorectal Carcinoma ◽

Survival Rates ◽

Elevated Serum ◽

Hepatic Metastases ◽

Lactic Dehydrogenase ◽

Serum Bilirubin Level ◽

Elevated Alkaline Phosphatase ◽

Multifactorial Analysis ◽

Primary Colorectal Tumor

A multifactorial analysis was used to identify the dominant prognostic variables predicting survival rates of 175 patients with hepatic metastases from colorectal carcinoma. Seven of 22 parameters examined simultaneously were found to independently influence the median survival rate in these patients: (1) elevated alkaline phosphatase (p = 0.0004), (2) elevated serum bilirubin level (p = 0.0005), (3) location of hepatic metastases (unilateral or bilateral, p = 0.0022), (4) number of metastatic nodes involved (0, 1-5, greater than 5; p = 0.0148), (5) depressed serum albumin (p = 0.0217), (6) whether or not the primary colorectal tumor was resected (p = 0.0013), and (7) chemotherapy (given or withheld, p = 0.0439). The prothrombin time, serum lactic dehydrogenase, and the number of hepatic metastases also correlated with survival, but they did not independently predict survival rates after other more dominant factors were accounted for. A mathematical equation for predicting an individual patient's clinical course once they developed hepatic metastases was derived from this statistical analysis. In addition, a simple and clinically useful guide for predicting outcome was developed that integrated the two most important risk factors, alkaline phosphatase and bilirubin.

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