Solubilized Rat Liver Vitamin K Carboxylase Demonstrates Little Selectivity between Vitamin K1 and the Menaquinones

Yen, C. S.; Mack, Donald O.

doi:10.3181/00379727-165-40975

Cited by 4 publications

(3 citation statements)

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“…Although some reports 22,23) suggest that MKs with long isoprenyl side chains, which showed lower levels in the cancerous liver tissue of our hepatocellular carcinoma patients, do not participate in γ-carboxylation, other reports [24][25][26][27] indicate that they do participate. Therefore, we believe that the low levels of MKs with long isoprenyl side chains in the cancerous tissue of hepatocellular carcinoma patients play a role in the serum PIVKA-II increase in these patients.…”

Section: Discussionmentioning

confidence: 69%

Vitamin K Contents in Liver Tissue of Hepatocellular Carcinoma Patients

Miyakawa

Kajiwara²,

Shirahata³

et al. 2000

Japanese Journal of Cancer Research

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Serum protein induced in vitamin K absence-II (PIVKA-II) is used as a tumor marker because it increases at a notably higher rate in patients with hepatocellular carcinoma. To clarify the mechanism causing the elevation of serum PIVKA-II, we measured the contents of vitamins K 1 (phylloquinone, PK) and K 2 (menaquinone, MK) (MK-4, MK-5, MK-6, MK-7, MK-8, MK-9, MK-10) in liver tissue resected from 21 hepatic cancer patients (12 patients with hepatocellular carcinoma and 9 patients with metastatic hepatic cancer), using HPLC combined with coulometric reduction and fluorometric detection. In the cancerous tissue of hepatocellular carcinoma patients, PK, MK-7, MK-8, and MK-10 were significantly lower than that found in the noncancerous tissue. Furthermore, MK-6, MK-7, MK-8, and MK-10 in the cancerous tissue of hepatocellular carcinoma patients were significantly lower than that in the cancerous tissue of metastatic hepatic cancer patients. These data suggested that one of the mechanisms of the elevation of serum PIVKA-II levels in hepatocellular carcinoma patients is a vitamin K deficiency in the local cancerous tissue.

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Section: Discussionmentioning

confidence: 69%

Vitamin K Contents in Liver Tissue of Hepatocellular Carcinoma Patients

Miyakawa

Kajiwara²,

Shirahata³

et al. 2000

Japanese Journal of Cancer Research

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“…Marked differences have been recognized between the fat-soluble and water-soluble K vitamins in Vitamin K and Benzo(a)pyrene Metabolism their metabolic activity that may relate to differences in penetration of and solubility in the microsomal membrane (24). There are also major differences in tissue distribution and clearance between vitamin K1 and K3.…”

Section: Discussionmentioning

confidence: 99%

“…24 h after the intravenous injection of vitamin K3 in rats 20% was excreted in urine and stool with <1% of the injected dose residual in liver and 10% in skeletal muscle (25). In the same study 6% of the injected dose of vitamin K1 was excreted in urine and stool with 20% remaining in liver and 7% in skeletal muscle 24 h postinjection (25). In man Bjornsson et al (26) found the turnover time of vitamin K1 to be -153 min and estimated the total body pool to be only -100…”

Section: Discussionmentioning

confidence: 99%

Vitamin K as a regulator of benzo(a)pyrene metabolism, mutagenesis, and carcinogenesis. Studies with rat microsomes and tumorigenesis in mice.

Israels¹,

Walls²,

Ollmann³

et al. 1983

J. Clin. Invest.

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A B S T R A C T Vitamin K3 inhibits the conversion of benzo(a)pyrene to its more polar metabolites in an in vitro rat liver microsomal system. Vitamin K3 also inhibits benzo(a)pyrene metabolism in rat liver fragments and reduces its mutagenicity in the Ames test. Higher concentrations of vitamin K3 are required to comparably reduce benzo(a)pyrene metabolism when the microsomal system has been induced with 3-methylcholanthrene. High pressure liquid chromatography analysis of the products of benzo(a)pyrene metabolism shows a uniform reduction of all the metabolic products. When tumors were induced in ICR/Ha female mice by the intraperitoneal injection of benzo(a)pyrene, those mice given vitamin K3 before or both before and after benzo(a)pyrene had a slower rate of tumor appearance and tumor death rate as compared with those receiving benzo(a)pyrene alone. However, vitamin K, increased the rate of tumor death while vitamin K deprivation and warfarin decreased the rate of tumor appearance and death in benzo(a)pyrene-injected mice.These studies indicate that vitamin K3 is an inhibitor of aryl hydrocarbon hydroxylase and reduces the carcinogenic and mutagenic metabolites in vitro, and inhibits benzo(a)pyrene tumorigenesis in vivo. That vitamin K, enhances the benzo(a)pyrene effect while warfarin and vitamin K deficiency inhibit benzo(a)pyrene tumorigenesis indicates that vitamin K1, vitamin K deprivation, or possibly blockade of its metabolic cycle also modulates benzo(a)pyrene metabolism in vivo but by a mechanism or at a site different from the vitamin K3 effect. The vitamin K series should be considered as capable of serving a regulatory func-

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Post-translational carboxylation of preprothrombin

Johnson¹

1981

The Biological Effects of Glutamic Acid and Its Derivatives

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Solubilized Rat Liver Vitamin K Carboxylase Demonstrates Little Selectivity between Vitamin K1 and the Menaquinones

Cited by 4 publications

References 0 publications

Vitamin K Contents in Liver Tissue of Hepatocellular Carcinoma Patients

Vitamin K Contents in Liver Tissue of Hepatocellular Carcinoma Patients

Vitamin K as a regulator of benzo(a)pyrene metabolism, mutagenesis, and carcinogenesis. Studies with rat microsomes and tumorigenesis in mice.

Post-translational carboxylation of preprothrombin

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