Urinary polyamine excretion as related to cell death and cell proliferation induced by carbon tetrachloride intoxication

Anehus, Siw; Yngner, Torsten; Engelbrecht, Claes; Hafströlm, L; Heby, Olle

doi:10.1016/0014-4800(83)90090-4

Cited by 6 publications

(2 citation statements)

References 23 publications

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“…The use of specific inhibitors of the biosynthetic enzymes of polyamines (ornithine decarboxylase, adenosylmethionine decarboxylase, spermine synthase, spermidine synthase) has revealed that an undisturbed synthesis of polyamines is a prerequisite for cell proliferation [Janne et al, 19911, and that, in proliferating tissues , polyamine concentration is usually elevated. Polyamine determination in biological specimens has been proposed as a potentially useful nonspecific marker of neoplasic disease [Umeki et al, 19881, but its value for cancer screening has not yet been established [Cohen, 19771. Polyamine excretion shows a circadian rhythm and has also been found to increase following nonmalignant cell destruction or proliferation, as in acute and chronic hepatic diseases [Anehus et al, 1983[Anehus et al, , 1986Hrushesky et al, 1983;Umeki et al, 19881. No information is available about the behavior of polyamine excretion in subjects exposed to genotoxic chemicals such as PAHs.…”

Section: Introductionmentioning

confidence: 99%

Tumor markers in serum, polyamines and modified nucleosides in urine, and cytogenetic aberrations in lymphocytes of workers exposed to polycyclic aromatic hydrocarbons

Buchet

Ferreira

Burrion

et al. 1995

American J Industrial Med

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Some polycyclic aromatic hydrocarbons (PAHs) such as benzo(a)pyrene and benzo(a)anthracene are well-established genotoxic agents. Long-term exposure to PAHs may lead to proliferative cell disorders in humans, predominantly in the skin, lung, and bladder. The concentration of several tumor markers in serum, of polyamines and modified nucleosides in urine, and of cytogenetic endpoints in peripheral lymphocytes (sister-chromatid exchanges, high frequency cells [HFC], and micronuclei) were measured in 149 male workers exposed to PAHs in two coke oven and one graphite electrode plants, and in 137 controls. We have assessed whether these biomarkers were related to several parameters reflecting exposure to PAHs, i.e., the sum of the airborne concentration of 13 PAHs, 1-hydroxypyrene (1-OHP) concentration in postshift urine, benzo(a)pyrene-diolepoxide adducts to hemoglobin (BPDE-Hb adducts), and duration of exposure, taking also into account several possible confounding factors. HFC was the biomarker most consistently associated with the intensity of current exposure to PAHs. Smoking exerts an independent effect on the same parameter. On the basis of the logistic regression between the prevalence of abnormal HFC values and PAHs in air and 1-OHP in postshift urine found in nonsmokers, it is suggested that the latter should be kept below 6.4 micrograms/m3 and 2.7 micrograms/g creatinine, respectively. No relationship was found between the cytogenetic effects and BPDE-Hb adducts although both parameters are statistically correlated with the airborne PAH level. Some tumor markers in serum (carcinoembryonic antigen, tissue polypeptide antigen, sialic acid) and the urinary concentration of some polyamines were correlated with either PAHs in air or 1-OHP in urine. The associations, however, were very weak which suggests that these biomarkers have limited practical value for the health surveillance of groups of workers exposed to genotoxic PAHs.

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Section: Introductionmentioning

confidence: 99%

Tumor markers in serum, polyamines and modified nucleosides in urine, and cytogenetic aberrations in lymphocytes of workers exposed to polycyclic aromatic hydrocarbons

Buchet

Ferreira

Burrion

et al. 1995

American J Industrial Med

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“…Polyamines in hepatocytes appear to leak easily from cells when they are damaged. 17 Polyamines, putrescine in particular, act as antiinflammatory agents in rats: is't9 Putrescine attenuates carrageenin-induced edemalSand it also weakens Dgalactosamine-induced acute liver failure. 19 These results suggest that the production of putrescine follows that of NLacetylspermidine and then putrescine in the liver may attenuate hepatocyte damage in patient with liver diseases.…”

Section: Discussionmentioning

confidence: 99%

Elevation of N1-acetylspermidine and putrescine in hepatic tissues of patients with fulminant hepatitis and liver cirrhosis

et al. 1994

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Hepatic polyamines were assayed in 15 patients with liver diseases, 5 with fulminant hepatitis (FH); 3 with exacerbated liver cirrhosis (ELC); and 7 with liver cirrhosis (LC). Hepatic putrescine and N1-acetylspermidine as percentages of total polyamines, were elevated and spermine was decreased in all 15 patients. The increase in hepatic N1-acetylspermidine levels appeared to be greater in patients with FH and ELC than in those with LC. These results suggest that the production of N1-acetylspermidine in human liver is closely associated with the induction of spermidine/spermine N1-acetyltransferase activity in liver diseases.

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Elevation of acetylpolyamine levels in mouse tissues, serum and urine after treatment with radical-producing drugs and lipopolysaccharide

et al. 1988

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Polyamines and acetylpolyamines were analyzed in the liver, spleen, lung, kidney, serum and urine by high-performance liquid chromatography on a column of cation-exchange resin after administering various cytotoxic substances to male mice. All of the compounds tested more or less affected the tissue levels of polyamines, including putrescine, spermidine, spermine and acetylpolyamines (N1-acetylspermidine and N1-acetylspermine). It was found that they were classified into two groups of substances: one group (including radical-producing drugs and lipopolysaccharide) which elevated the tissue levels of N1-acetylspermidine, especially in the liver, while another group of drugs (such as D-galactosamine and DL-ethionine) had little effect on the acetylpolyamine levels. When the acetylpolyamine levels rose, the levels of spermidine and spermine declined, and then putrescine levels were elevated. N1-Acetylspermine was detected only when N1-acetylspermidine levels were very high after treatment with radical-producing drugs and lipopolysaccharide. Halogenated carbon, such as carbon tetrachloride and halothane, elevated the levels of acetylpolyamines especially in the liver, while paraquat elevated them in all tissues examined.

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Urinary polyamine excretion as related to cell death and cell proliferation induced by carbon tetrachloride intoxication

Cited by 6 publications

References 23 publications

Tumor markers in serum, polyamines and modified nucleosides in urine, and cytogenetic aberrations in lymphocytes of workers exposed to polycyclic aromatic hydrocarbons

Tumor markers in serum, polyamines and modified nucleosides in urine, and cytogenetic aberrations in lymphocytes of workers exposed to polycyclic aromatic hydrocarbons

Elevation of N1-acetylspermidine and putrescine in hepatic tissues of patients with fulminant hepatitis and liver cirrhosis

Elevation of acetylpolyamine levels in mouse tissues, serum and urine after treatment with radical-producing drugs and lipopolysaccharide

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