Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:6.3.4.6 (
urease
)
7,490
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Meralluride, mercaptomerin, ethacrynic acid, and penicillamine inhibited
urease
activity of Proteus mirabilis. The activity of the organic mercurials and ethacrynic acid was markedly inhibited by human and dog urine. Antiurease activity could not be detected in the urine of a human and a dog given meralluride by injection. Urine from patients receiving penicillamine also failed to inhibit
urease
activity.
Ascorbic acid
inhibited, whereas dehydroascorbic acid enhanced, the activity of the mercurials, but neither agent altered the inhibitory effect of urine. The lethal effect of meralluride against Proteus occurred at the same concentration at which
urease
activity was inhibited, but penicillamine inhibited the enzymatic activity without affecting viability of the organism. The data suggest that these sulfhydryl-reactive compounds will not be useful against Proteus infections of the urinary tract.
...
PMID:Effect of organic mercurials and sulfhydryl compounds on the urease activity of Proteus: inhibition by urine and ascorbic acid. 1 Aug 28
Free radicals (FRs) play an important role in the pathogenesis of gastroduodenal mucosal inflammation, peptic ulcer disease, and probably even gastric cancer. Various micronutrients protect the gastric mucosa by scavenging FRs. Only limited data is available regarding the concentration of micronutrients in the gastric mucosa in patients with gastritis and peptic ulcer disease. Our aim was to analyze micronutrient antioxidant concentrations in the antral mucosa in patients with gastritis and gastric ulcer and to determine the influence of Helicobacter pylori infection on gastric mucosal antioxidants in patients with gastritis and gastric ulcer. Patients who underwent upper endoscopy for evaluation of dyspepsia were included in the study.
Ascorbic acid
, alpha-tocopherol, alpha-carotene, beta-carotene, total carotenoids, lutein, cryptoxanthin, and lycopene levels were measured in the sera and antral mucosal biopsies in these patients. The diagnosis of H. pylori was confirmed by histology,
urease
test (CLO) and serology. Patients with negative endoscopic findings and normal histology and no H. pylori infection served as controls. In patients with gastritis, alpha-tocopherol levels were reduced in serum and mucosa irrespective of H. pylori status, whereas carotenoids and ascorbic acid levels were similar to controls. However, in patients with gastric ulcer, serum and mucosal levels of all micronutrient antioxidants were markedly decreased compared with both controls and patients with gastritis. The degree of depletion of antioxidants was similar in patients with either H. pylori-induced or nonsteroidal antiinflammatory drug (NSAID)-induced ulcers. Patients with gastric ulcer have very low gastric antioxidant concentrations compared to patients with gastritis and normal mucosa. This depletion in antioxidants seems to be a nonspecific response and was not related to H. pylori infection.
...
PMID:Micronutrient antioxidants in gastric mucosa and serum in patients with gastritis and gastric ulcer: does Helicobacter pylori infection affect the mucosal levels? 1115 82
Potential of nonantibiotic therapies for treatment of Helicobacter pylori-related acid peptic disease remains underexplored. Several clinical studies have shown that higher prevalence of H. pylori infection is associated with low
Vitamin C
(Vit C) level in serum and gastric juice. However, there is no consensus regarding the usefulness of Vit C supplementation in the management of H. pylori infection. Surveying the existing literature we conclude that high concentration of Vit C in gastric juice might inactivate H. pylori
urease
, the key enzyme for the pathogen's survival and colonization into acidic stomach. Once infection established,
urease
is not very important for its survival. The role of Vit-C as anti-H. pylori agent in peptic ulcer diseases appears to be preventive rather than curative. Rather than supplementing high dose of Vit C along with conventional triple therapy, it is preferable to complete the conventional therapy and thereafter start Vit C supplementation for extended period which would prevent reinfection in susceptible individuals, provided the patients are not achlorhydric. Further studies are required to prove the role of Vit C in susceptible population.
...
PMID:Vitamin-C as anti-Helicobacter pylori agent: More prophylactic than curative- Critical review. 2214 62
The treatment of
Helicobacter pylori
(
H. pylori
) induced infections using antibiotic therapies is clinically well accepted; however, using a noninvasive approach with the implementation of therapeutic agents such as vitamin C is not well investigated.
Vitamin C
has certain characteristics, which allow for it to be considered as a potential treatment option for patients with
H. pylori
infections.
Vitamin C
's hostility and mechanism of action towards
H. pylori
infection in peptic ulcer disease can be classified into two categories: as a preventative agent and alternatively as a therapeutic agent. Preventatively vitamin C acts as a biological antioxidant as well as an immune boosting agent, while therapeutically it acts as an inhibitor of
urease
, a potential collagen synthesizing agent, and a stimulant in prostaglandin synthesis. As a result, the dosage of vitamin C should be highly regulated. Furthermore, numerous studies have shown that vitamin C supplementation if taken with antibiotics can increase the efficiency of the treatment leading to an increased possibility of eradication of
H. pylori
in infected individuals. This paper will investigate the recent studies that show different mechanisms through which vitamin C can be used as a preventative or a therapeutic agent for the treatment of
H. pylori
related infections.
...
PMID:Vitamin C: A Preventative, Therapeutic Agent Against Helicobacter pylori. 3028 58