Effect of protein-free diet on UDP-glucuronyltransferase and sulphotransferase activities in rat liver

Woodcock, Barry G.; Wood, G. C.

doi:10.1016/0006-2952(71)90180-8

Cited by 57 publications

(32 citation statements)

References 18 publications

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“…Acute treatment with endotoxin to the low protein diet rats further significantly decreased MFO enzymes except cytochrome P-450 levels from the normal diet control group. Hepatic microsomal pnitrophenol glucuronidation was signifi cantly increased in animals fed low protein diet, which is in agreement with previous observations of Woodcock and Wood [33]. However, liver microsomal p-nitrophenol-UDP-glucuronyltransferasc activity was not altered by endotoxin treatment, which is in contrast to our previous observations [11].…”

Section: Discussioncontrasting

confidence: 57%

Endotoxin and Low Protein Diet Induced Depression of the Rat Hepatic Drug Metabolism

Sonawane¹,

Yaffe²

1983

Pharmacology

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The effects of the combination of low protein diet feeding and endotoxin (E. coli, serotype 026 B6) upon rat hepatic microsomal mixed function oxidase (MFO) enzymes were investigated. Short-term (7 days) feeding of low protein (8 %) diet and acute (single dose) exposure to endotoxin resulted in an additive decrease in MFO enzymes. However, chronic (7 days) endotoxin exposure did not depress liver microsomal MFO enzyme activities except for aniline hydroxylase. Long-term (105 days) feeding of the low protein diet and acute endotoxin exposure further decreased aminopyrine N-demethylase and benzo(a)pyrene hydroxylase activities compared to individual treatments. These results suggest that, under these experimental conditions, the two host-related environmental factors interact and potentiate a decrease in rat hepatic microsomal drug metabolizing enzymes. These observations may be of clinical relevance to explain altered drug reactions in patients with gram-negative infections and endotoxemia under the conditions of malnutrition.

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Section: Discussioncontrasting

confidence: 57%

Endotoxin and Low Protein Diet Induced Depression of the Rat Hepatic Drug Metabolism

Sonawane¹,

Yaffe²

1983

Pharmacology

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“…Uridine diphosphoglucuronyl transferase activity: This assay was done using p-nitrophenyl phosphate (PNP) as the substrate according to the modified method of Woodcock and Wood (Woodcock and Wood, 1971). The reaction mixture had 0.4 ml total volume containing 0.1 M Tris Hcl (pH 8.5), 4 mM magnesium chloride, 0.5 mM PNP, 2 mM UDPGA and 50 µl of the microsomal fraction.…”

Section: Glutathione -S-transferase Activity: Gst Activity Was Purplementioning

confidence: 99%

Purple Rice Extract Supplemented Diet Reduces DMH-Induced Aberrant Crypt Foci in the Rat Colon by Inhibition of Bacterial β-Glucuronidase

Summart

Chewonarin²

2014

Asian Pacific Journal of Cancer Prevention

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Background: Purple rice has become a natural product of interest which is widely used for health promotion. This study investigated the preventive effect of purple rice extract (PRE) mixed diet on DMH initiation of colon carcinogenesis. Materials and Methods: Rats were fed with PRE mixed diet one week before injection of DMH (40 mg/kg of body weight once a week for 2 weeks). They were killed 12 hrs after a second DMH injection to measure the level of O 6-methylguanine and xenobiotic metabolizing enzyme activities. Results: In rats that received PRE, guanine methylation was reduced in the colonic mucosa, but not in the liver, whereas PRE did not affect xenobiotic conjugation, with reference to glutathione-S-transferase or UDP-glucuronyl transferase. After 5 weeks, rats that received PRE with DMH injection had fewer ACF in the colon than those treated with DMH alone. Interestingly, a PRE mixed diet inhibited the activity of bacterial β-glucuronidase in rat feces, a critical enzyme for free methylazoxymethanol (MAM) release in the rat colon. These results indicated that purple rice extract inhibited β-glucuronidase activity in the colonic lumen, causing a reduction of MAM-induced colonic mucosa DNA methylation, leaded to decelerated formation of aberrant crypt foci in the rat colon. Conclusions: The supplemented purple rice extract might thus prevent colon carcinogenesis by the alteration of the colonic environment, and thus could be further developed for neutraceutical products for colon cancer prevention.

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“…Assays were carried out to evaluate the activities of the following Phase I and II enzymes of xenobiotic metabolism: Activating (Phase I) enzyme systems, (i) cytochrome P-450 [13]; (ii) aryl hydrocarbon hydroxylase (modified radiometric method of DePierre et al [14]; (iii) aminopyrine demethylase, with aminopyrine used as substrate [15]; (iv) microsomal epoxide hydrolase, with benzo(a)pyrene-4,5-oxide as substrate [16]; (v) aniline hydroxylase, with aniline as substrate [15]. Conjugating (Phase II) enzyme systems, (i) uridine diphosphoglucuronyl transferase, with p-nitrophenol as substrate [17]; (ii) glutathione-S-transferase, with 1-chloro-2,4-dinitrobenzene as substrate [18]. Protein estimations in microsomal and cytosolic fractions were carried out by the method of Lowry et al [19].…”

Section: Methodsmentioning

confidence: 99%

Activities of Carcinogen Metabolizing Enzymes in Hepatic and Extra Hepatic Tissues of Iron-Deficient Rats.

Rao¹,

Vaidyanathan²

1994

J. Clin. Biochem. Nutr.

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SummaryThe effect of iron deficiency on the activities of xenobiotic metabolizing enzymes, both activating (Phase I) and conjugating (Phase II), was studied in an experimental system. A group of male weanling Fischer rats was fed a casein sucrose starch-based diet devoid of iron for a period of 6 weeks. Another group of rats, which received an ironsufficient diet, was used as the control. Hematological investigations on hemoglobin, protoporphyrin/heme ratio, and serum iron confirmed the development of iron deficiency in the experimental group by 6 weeks. At the end of the experimental period, microsomes and cytosolic preparations were made from various tissues that are sites of drug metabolism, i.e., liver, kidneys, lungs, and intestinal mucosa. Activities of many enzymes of Phase I, like cytochrome P-450, aryl hydrocarbon hydroxylase, aminopyrine demethylase, aniline hydroxylase and microsomal epoxide hydrolase and of Phase II, like uridine diphosphoglucuronyl transferase and glutathione-S-transferase, were investigated. The results showed that the activities of aminopyrine demethylase, aniline hydroxylase, and microsomal epoxide hydrolase among the activating enzymes and uridine diphosphoglucuronyl transferase, a conjugating enzyme, were significantly decreased in iron deficiency. An impairment in detoxification of ingested xenobiotics is thus indicated in iron deficiency. This might lead to the persistence of ingested compounds in the body without elimination, which might prove to be harmful to the host. Formation of electrophilic metabolites without subsequent removal may result in the formation of DNA adducts, which is a necessary step in chemical carcinogenesis.

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Effect of protein-free diet on UDP-glucuronyltransferase and sulphotransferase activities in rat liver

Cited by 57 publications

References 18 publications

Endotoxin and Low Protein Diet Induced Depression of the Rat Hepatic Drug Metabolism

Endotoxin and Low Protein Diet Induced Depression of the Rat Hepatic Drug Metabolism

Purple Rice Extract Supplemented Diet Reduces DMH-Induced Aberrant Crypt Foci in the Rat Colon by Inhibition of Bacterial β-Glucuronidase

Activities of Carcinogen Metabolizing Enzymes in Hepatic and Extra Hepatic Tissues of Iron-Deficient Rats.

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