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Enzyme
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Target Concepts:
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Query: EC:3.6.3.1 (
Mg2+-ATPase
)
1,484
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The aim of our work is to show the importance of the role of hydrophobic bonds in maintaining
Mg2+-ATPase
or sucrase activity and Na+-coupled D-glucose uptake normal for the
brush border
of rat enterocytes. The activity of the two enzymes and the D-glucose uptake were therefore measured under the action of n-aliphatic alcohols and related to the fluidity determined by ESR. Three concentrations were used for the first eight alcohols, those of octanol being about 1500-times lower than those of methanol. For each alcohol the D-glucose uptake and the fluidity were linear functions of the logarithm of the concentration, the linear regressions being practically parallel and equidistant. The concentrations (C) of the eight alcohols inhibiting the D-glucose uptake by 80% were similar to those increasing the membrane fluidity by 3%. The linear relationship which existed in both cases between log 1/C and log P, P being octanol/water partition coefficients of the alcohols, was evidence of great sensitivity to the hydrophobic effect of the alcohols. Only the first alcohols, however, produced any notable inhibition of
Mg2+-ATPase
and sucrase. Hydrophobic bonds are thus shown to have little influence in maintaining the activity of
Mg2+-ATPase
and sucrase, but they modulate the Na+-coupled D-glucose uptake.
...
PMID:Sensitivity of Na+-coupled D-glucose uptake, Mg2+-ATPase and sucrase to perturbations of the fluidity of brush-border membrane vesicles induced by n-aliphatic alcohols. 614 7
The effect of a single oral dose of malathion (1 g/kg body wt.) on the digestive and absorptive functions of the intestinal epithelium has been investigated in rats. The absorption of glucose and glycine was considerably reduced (35%) inpesticide fed animals compared to controls. The activities of
brush border
sucrase, lactase, alkaline phosphatase,
Mg2+-ATPase
and lactate dehydrogenase were also significantly depressed in malathion exposed rats, but there was no change in the leucine aminopeptidase levels under these conditions. Mucosal DNA, RNA and protein contents remained unaltered in pesticide toxicity. These results suggest that malathion toxicity induces functional derangements of the intestine.
...
PMID:Effect of a single oral dose of malathion on D-glucose and glycine uptake and on brush border enzymes in rat intestine. 744 81
Carcinogenic and other toxic manifestations of areca/betel nut extracts on the buccal cavity and upper digestive tract are well documented. The present study deals with in vivo and in situ effects of aqueous and alcoholic extracts of areca nut on rat intestinal epithelial cell membrane. In vivo daily oral administration by gastric intubation for 1p w produced significant declines in
brush border
membrane alkaline phosphatase, Ca2+-
Mg2+-ATPase
, and the digestive enzyme sucrase. The decline in activities were more prominent after 4-w exposures. Instant short term in situ exposure to aqueous extract produced higher enzyme activities, indicating the initial activation of active sites by areca nut extract constituent(s). Significant declines in
brush border
membrane constituents (total hexose, sialic acid and cholesterol) were also evident following continuous exposures to areca nut extracts. These findings suggest that prolonged chewing of areca nut causes significant alterations in intestinal epithelial cell lining functions and could lead to malabsorption of nutrients.
...
PMID:Effect of betel/areca nut (Areca catechu) extracts on intestinal epithelial cell lining. 1100 13
Bile is a complex mixture that includes bile salts, the membrane phospholipid phosphatidylcholine (PC), cholesterol and various endobiotic and xenobiotic toxins, each of which is secreted across the canalicular membrane of the hepatocyte by different ATP-binding cassette (ABC) transporters. The bile salts are essential for the emulsification of dietary fat and lipophilic vitamins. They are synthesized from cholesterol in the hepatocyte and their secretion by the bile salt export pump (BSEP or ABCB11) drives bile flow and is the starting point for the enterohepatic cycle. The detergent nature of bile salts that is key to their physiological role also means that they are inherently cytotoxic, and failure to secrete bile (intraheptic cholestasis) can precipitate severe liver disease and mortality. Such progressive familial intrahepatic cholestasis (PFIC) comes in three types of autosomal recessive disease. PFIC2 is caused by mutation to ABCB11. PFIC3 is caused by mutation of a closely related ABC transporter, ABCB4, which flops PC into the outerleaflet of the canalicular membrane. The flopped PC is extracted by the bile salts in the canaliculus to form a mixed micelle that reduces bile salt detergent activity. The third protein that is essential for bile flow from the hepatocyte is a member of a different class of transporter protein, a P-type ATPase, ATP8B1. Mutation of ATP8B1 causes PFIC1, but ATP8B1 does not transport a component of bile into the canaliculus. Data from different laboratories, published this year, suggests two different roles for ATP8B1 in the hepatocyte: a lipid
flippase
, that counterbalances the deleterious effects of ABCB4 on barrier function of the canalicular membrane; and an anchor of the actin cytoskeleton necessary to form the microvilli of the
brush border
. These latest discoveries are described, along with a spectrum of cholestatic disorders whose aetiologies lie in these and other transporters of the canalicular membrane.
...
PMID:Canalicular ABC transporters and liver disease. 2198 74
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