carcinogenesis/albumin

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The catalytic effect of bovine serum albumin on the ortho rearrangement of the potential ultimate carcinogen, N-(sulfooxy)-2-(acetylamino)fluorene, generated enzymatically from N-hydroxy-2-(acetylamino)fluorene and evidence for substrate specificity of the enzymatic sulfonation of arylhydroxamic acids.

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This investigation examines the catalytic effect of bovine serum albumin on the ortho rearrangement of the possible ultimate carcinogen, N-(sulfooxy)-2-(acetylamino)fluorene, generated from N-hydroxy-2-(acetylamino)fluorene by the sulfotransferase(s) in the cytosol of rat liver. With various

Molecular dosimetry of the food-borne carcinogen MeIQx using adducts of serum albumin.

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Incubation of mouse serum albumin with the food borne carcinogen [2-14C]-Amino-3,8,-dimethylimidazo[4,5-f]quinoxaline (14C-MeIQx) in the presence of mouse hepatic microsomes and an NADPH-regenerating system in vitro resulted in the formation of adducts of MeIQx with albumin, which increased

Albumin-negative hepatocytes in Sprague-Dawley x analbuminemic F1 rats treated with hepatic carcinogens.

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Analbuminemic rats (NAR) are a mutant breed with an inherent inability to synthesize albumin. However, heterozygous rats born of a pair of NAR and Sprague-Dawley (SD) rats can synthesize albumin. Immunohistochemical staining for albumin shows that, although the majority of hepatocytes of SD x NAR F1

Sequence content of alpha-fetoprotein, albumin and fibrinogen polypeptide mRNAs in different organs, developing tissues and in liver during carcinogenesis in rats.

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To investigate the variable gene activities of alpha-fetoprotein, albumin and fibrinogen polypeptides as markers of 'liver specific proteins' in different developing organs or tissues, we have used specific complementary DNA probes to detect and to quantitate alpha-fetoprotein, albumin and

Mapping serum albumin adducts of the food-borne carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine by data-dependent tandem mass spectrometry.

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2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a heterocyclic aromatic amine that is formed during the cooking of meats. PhIP is a potential human carcinogen: it undergoes metabolic activation to form electrophilic metabolites that bind to DNA and proteins, including serum albumin (SA).

Biomonitoring an Albumin Adduct of the Cooked Meat Carcinogen 2-Amino-1-Methyl-6-Phenylimidazo[4,5-b]pyridine in Humans.

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2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is formed in cooked meats and may be linked to dietary associated colorectal, prostate, and mammary cancers. Genotoxic N-oxidized metabolites of PhIP react with the Cys 34 of albumin (Alb) to form a sulfinamide adduct, a biomarker of the

Optimizing proteolytic digestion conditions for the analysis of serum albumin adducts of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, a potential human carcinogen formed in cooked meat.

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Heterocyclic aromatic amines (HAAs) are carcinogens formed during the cooking of meats or arise in tobacco smoke. The genotoxic N-oxidized metabolites of HAAs bind to Cys residues of proteins to form arylsulfinamide adducts. However, these adducts are unstable and undergo hydrolysis during enzymatic

Competitive interactions of anti-carcinogens with serum albumin: a spectroscopic study of bendamustine and dexamethasone with the aid of chemometrics.

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Interactions between the anti-carcinogens, bendamustine (BDM) and dexamethasone (DXM), with bovine serum albumin (BSA) were investigated with the use of fluorescence and UV-vis spectroscopies under pseudo-physiological conditions (Tris-HCl buffer, pH 7.4). The static mechanism was responsible for

Aflatoxin-albumin adducts: a basis for comparative carcinogenesis between animals and humans.

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The study objectives were (a) to correlate AFB1 serum albumin adduct levels with AFB1-DNA adduct levels in liver in different rodent species to determine whether the former could serve as a marker of hepatic DNA adduct levels irrespective of species, and (b) to relate the levels of both adducts to

Agnostic Cys34-albumin adductomics and DNA methylation: implication of N-acetylcysteine in lung carcinogenesis years before diagnosis.

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Although smoking and oxidative stress are known contributors to lung carcinogenesis, their mechanisms of action remain poorly understood. To shed light into these mechanisms, we applied a novel approach using Cys34-adductomics in a lung cancer nested case-control study (n=212). Adductomics profiles

alpha-Fetoprotein and albumin mRNA levels in liver regeneration and carcinogenesis.

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Using a titration procedure, we measured the proportion of alpha-fetoprotein (AFP) and albumin mRNA in normal, regenerating, and preneoplastic rat livers. AFP mRNA constitutes approximately 0.006% of the polysomal polyadenylated RNA of normal livers and this proportion increases only slightly before

alpha-Fetoprotein and albumin genes of rats: no evidence for amplification-deletion or rearrangement in rat liver carcinogenesis.

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Full-length radiolabeled albumin and alpha-fetoprotein (AFP) cDNAs were synthesized from pure albumin and AMP mRNA preparations by using avian myeloblastosis virus reverse transcriptase (RNA-dependent DNA polymerase). The cDNAs have been used to quantitate the number of albumin and AFP genes in

Characterization of rare p53 mutants from carcinogen-treated albumin-simian virus 40 T-antigen transgenic rats.

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The p53 gene has been either mutated or deleted in most human tumors examined to date. Mutations in the specific DNA-binding domain are the most common p53 mutations and are of interest because they may produce p53 molecules with transcriptional capabilities unlike those of the wild-type (WT) p53

Structural changes in albumin are a possible mechanism for fluctuation of cefazorin and ibuprofen plasma protein binding in rats with carcinogen-induced osteosarcoma.

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OBJECTIVE It is known that the protein-unbound fraction (fp) of warfarin fluctuates in the plasma of cancer patients and the fluctuation of fp is correlated with albumin concentration. However, this mechanism remains unclear. The present study was performed with the objective of elucidating

Serum albumin adducts in the molecular epidemiology of aflatoxin carcinogenesis: correlation with aflatoxin B1 intake and urinary excretion of aflatoxin M1.

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Aflatoxin-serum albumin adducts in the blood of 42 residents of Guangxi Province, People's Republic of China, were determined and compared with intake of aflatoxin B1 (AFB1) and excretion of aflatoxin M1 (AFM1) in urine. Blood specimens were obtained during the same period that urine was collected

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