Serum Epoxide Hydrolase (Preneoplastic Antigen) in Human and Experimental Liver Injur

David E. Moody; Dana N. Loury; Bruce D. Hammock; Boris H. Ruebner; John M. Cullen; James H. Hillman; David W. Hillman; M. Sambasiva Rao; W. Thomas London; Hei Won L. Hann; Irving Millman; Martin J. Griffin; Dana N. Loury; John M. Cullen; Hei Won L. Hann; Martin J. Griffin

Serum Epoxide Hydrolase (Preneoplastic Antigen) in Human and Experimental Liver Injur

David E. Moody^*, Dana N. Loury, Bruce D. Hammock, Boris H. Ruebner, John M. Cullen, James H. Hillman, David W. Hillman, M. Sambasiva Rao, W. Thomas London, Hei Won L. Hann, Irving Millman, Martin J. Griffin, Dana N. Loury, John M. Cullen, Hei Won L. Hann, Martin J. Griffin

^*Corresponding author for this work

Pathology

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Abstract

Reports of an increase in a serum epoxide hydrolase (sEH), immunochemically related to microsomal EH in humans and rats with hepatocellular carcinoma (HCC), suggested its use as a serum marker for this disease. We have now measured sEH levels (as either immunochemically determined content or enzyme activity) in a number of human and experimental models of liver disease. sEH was elevated above the normal range in at least 50% of individuals with HCC, including: 3 of 6 northern Californians; 4 of 7 Koreans with hepatitis B-associated HCC; hepatitis B-associated HCC in woodchucks; and male rats receiving chronic treatment with aflatoxin B, or ciprofibrate. sEH was rarely elevated in other forms of chronic liver disease. Only 2 of 9 Koreans with hepatitis B-associated cirrhosis, 1 of 8 carriers, but none with chronic active hepatitis or infection with no apparent liver disease had elevated sEH. In addition, no elevations were found in woodchucks with noncancerous viral hepatitis. In aflatoxin B1- and M1-treated rats sEH was not elevated in those with only hyperplastic foci or hepatocellular adenomas, and in two rat initiationpromotion protocols sEH was elevated only in those rats which received the entire set of treatments. sEH was also increased during acute hepatotoxicity in rats treated with Cd4 or 1,2-dibromo-3-chloropropane. The mechanism of increase in sEH during hepatocarcinogenesis appears to be different from that of other markers of HCC, for in the Korean patients, there was no correlation between sEH concentrations and those of α-fetoprotein or ferritin, nor was there a correlation with α-fetoprotein concentrations in the aflatoxin-treated rats. Furthermore, the increase in sEH does not correlate with induction of microsomal (H in the liver of experimental animals. Studies to date indicate that sEH is selective for HCC and severe hepatonecrotic injury, and may be of some use in the diagnosis of HCC, particularly as a complement to other serum markers.

Original language	English (US)
Pages (from-to)	395-403
Number of pages	9
Journal	Cancer Epidemiology Biomarkers and Prevention
Volume	1
Issue number	5
State	Published - 1992

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Epidemiology
Oncology

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Moody, D. E., Loury, D. N., Hammock, B. D., Ruebner, B. H., Cullen, J. M., Hillman, J. H., Hillman, D. W., Rao, M. S., London, W. T., Hann, H. W. L., Millman, I., Griffin, M. J., Loury, D. N., Cullen, J. M., Hann, H. W. L., & Griffin, M. J. (1992). Serum Epoxide Hydrolase (Preneoplastic Antigen) in Human and Experimental Liver Injur. Cancer Epidemiology Biomarkers and Prevention, 1(5), 395-403.

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title = "Serum Epoxide Hydrolase (Preneoplastic Antigen) in Human and Experimental Liver Injur",

abstract = "Reports of an increase in a serum epoxide hydrolase (sEH), immunochemically related to microsomal EH in humans and rats with hepatocellular carcinoma (HCC), suggested its use as a serum marker for this disease. We have now measured sEH levels (as either immunochemically determined content or enzyme activity) in a number of human and experimental models of liver disease. sEH was elevated above the normal range in at least 50% of individuals with HCC, including: 3 of 6 northern Californians; 4 of 7 Koreans with hepatitis B-associated HCC; hepatitis B-associated HCC in woodchucks; and male rats receiving chronic treatment with aflatoxin B, or ciprofibrate. sEH was rarely elevated in other forms of chronic liver disease. Only 2 of 9 Koreans with hepatitis B-associated cirrhosis, 1 of 8 carriers, but none with chronic active hepatitis or infection with no apparent liver disease had elevated sEH. In addition, no elevations were found in woodchucks with noncancerous viral hepatitis. In aflatoxin B1- and M1-treated rats sEH was not elevated in those with only hyperplastic foci or hepatocellular adenomas, and in two rat initiationpromotion protocols sEH was elevated only in those rats which received the entire set of treatments. sEH was also increased during acute hepatotoxicity in rats treated with Cd4 or 1,2-dibromo-3-chloropropane. The mechanism of increase in sEH during hepatocarcinogenesis appears to be different from that of other markers of HCC, for in the Korean patients, there was no correlation between sEH concentrations and those of α-fetoprotein or ferritin, nor was there a correlation with α-fetoprotein concentrations in the aflatoxin-treated rats. Furthermore, the increase in sEH does not correlate with induction of microsomal (H in the liver of experimental animals. Studies to date indicate that sEH is selective for HCC and severe hepatonecrotic injury, and may be of some use in the diagnosis of HCC, particularly as a complement to other serum markers.",

author = "Moody, {David E.} and Loury, {Dana N.} and Hammock, {Bruce D.} and Ruebner, {Boris H.} and Cullen, {John M.} and Hillman, {James H.} and Hillman, {David W.} and Rao, {M. Sambasiva} and London, {W. Thomas} and Hann, {Hei Won L.} and Irving Millman and Griffin, {Martin J.} and Loury, {Dana N.} and Cullen, {John M.} and Hann, {Hei Won L.} and Griffin, {Martin J.}",

year = "1992",

language = "English (US)",

volume = "1",

pages = "395--403",

journal = "Cancer Epidemiology Biomarkers and Prevention",

issn = "1055-9965",

publisher = "American Association for Cancer Research Inc.",

number = "5",

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T1 - Serum Epoxide Hydrolase (Preneoplastic Antigen) in Human and Experimental Liver Injur

AU - Moody, David E.

AU - Loury, Dana N.

AU - Hammock, Bruce D.

AU - Ruebner, Boris H.

AU - Cullen, John M.

AU - Hillman, James H.

AU - Hillman, David W.

AU - Rao, M. Sambasiva

AU - London, W. Thomas

AU - Hann, Hei Won L.

AU - Millman, Irving

AU - Griffin, Martin J.

AU - Loury, Dana N.

AU - Cullen, John M.

AU - Hann, Hei Won L.

AU - Griffin, Martin J.

PY - 1992

Y1 - 1992

N2 - Reports of an increase in a serum epoxide hydrolase (sEH), immunochemically related to microsomal EH in humans and rats with hepatocellular carcinoma (HCC), suggested its use as a serum marker for this disease. We have now measured sEH levels (as either immunochemically determined content or enzyme activity) in a number of human and experimental models of liver disease. sEH was elevated above the normal range in at least 50% of individuals with HCC, including: 3 of 6 northern Californians; 4 of 7 Koreans with hepatitis B-associated HCC; hepatitis B-associated HCC in woodchucks; and male rats receiving chronic treatment with aflatoxin B, or ciprofibrate. sEH was rarely elevated in other forms of chronic liver disease. Only 2 of 9 Koreans with hepatitis B-associated cirrhosis, 1 of 8 carriers, but none with chronic active hepatitis or infection with no apparent liver disease had elevated sEH. In addition, no elevations were found in woodchucks with noncancerous viral hepatitis. In aflatoxin B1- and M1-treated rats sEH was not elevated in those with only hyperplastic foci or hepatocellular adenomas, and in two rat initiationpromotion protocols sEH was elevated only in those rats which received the entire set of treatments. sEH was also increased during acute hepatotoxicity in rats treated with Cd4 or 1,2-dibromo-3-chloropropane. The mechanism of increase in sEH during hepatocarcinogenesis appears to be different from that of other markers of HCC, for in the Korean patients, there was no correlation between sEH concentrations and those of α-fetoprotein or ferritin, nor was there a correlation with α-fetoprotein concentrations in the aflatoxin-treated rats. Furthermore, the increase in sEH does not correlate with induction of microsomal (H in the liver of experimental animals. Studies to date indicate that sEH is selective for HCC and severe hepatonecrotic injury, and may be of some use in the diagnosis of HCC, particularly as a complement to other serum markers.

AB - Reports of an increase in a serum epoxide hydrolase (sEH), immunochemically related to microsomal EH in humans and rats with hepatocellular carcinoma (HCC), suggested its use as a serum marker for this disease. We have now measured sEH levels (as either immunochemically determined content or enzyme activity) in a number of human and experimental models of liver disease. sEH was elevated above the normal range in at least 50% of individuals with HCC, including: 3 of 6 northern Californians; 4 of 7 Koreans with hepatitis B-associated HCC; hepatitis B-associated HCC in woodchucks; and male rats receiving chronic treatment with aflatoxin B, or ciprofibrate. sEH was rarely elevated in other forms of chronic liver disease. Only 2 of 9 Koreans with hepatitis B-associated cirrhosis, 1 of 8 carriers, but none with chronic active hepatitis or infection with no apparent liver disease had elevated sEH. In addition, no elevations were found in woodchucks with noncancerous viral hepatitis. In aflatoxin B1- and M1-treated rats sEH was not elevated in those with only hyperplastic foci or hepatocellular adenomas, and in two rat initiationpromotion protocols sEH was elevated only in those rats which received the entire set of treatments. sEH was also increased during acute hepatotoxicity in rats treated with Cd4 or 1,2-dibromo-3-chloropropane. The mechanism of increase in sEH during hepatocarcinogenesis appears to be different from that of other markers of HCC, for in the Korean patients, there was no correlation between sEH concentrations and those of α-fetoprotein or ferritin, nor was there a correlation with α-fetoprotein concentrations in the aflatoxin-treated rats. Furthermore, the increase in sEH does not correlate with induction of microsomal (H in the liver of experimental animals. Studies to date indicate that sEH is selective for HCC and severe hepatonecrotic injury, and may be of some use in the diagnosis of HCC, particularly as a complement to other serum markers.

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Serum Epoxide Hydrolase (Preneoplastic Antigen) in Human and Experimental Liver Injur

Abstract

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ASJC Scopus subject areas

UN SDGs

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