Disease relevance of Benzydyna

• Clones of Friend erythroleukemia cells, characterized by the presence of 40-70% benzidine-positive cells synthesizing hemoglobin in the absence of inducing drugs, were treated with several phorbol diesters with a known range of tumor-promoting activity on mouse skin [1].
• Depending upon experimental conditions, benzidine treatment effected development of liver tumors, lung adenomas [2].
• In addition, benzidine exposure was found to decrease host resistance, including resistance to the growth of transplantable tumor cells and infection with Listeria [3].
• Prostaglandin H synthase supports the activation of benzidine to a mutagenic species in the Ames (Salmonella typhimurium) test, and our studies of the mechanism of this activation are described [4].
• The correlation between DNA adducts and chromosomal aberrations in the target organ of benzidine exposed, partially-hepatectomized mice [5].

High impact information on Benzydyna

• A factor from conditioned medium of a leukaemia cell line has been isolated which can induce mouse Friend cells to become benzidine-positive, and which shares a similar N-terminal sequence with porcine FRP [6].
• Risk of bladder tumors among benzidine workers and their serum properdin levels [7].
• IS cells did not have the character of erythroid cells: They did not contain detectable heme as measured by benzidine-peroxide reagent, did not contain globin mRNA in detectable amounts, and did not produce erythroid colonies in plasma culture in the absence or presence of erythropoietin [8].
• Suppression of K562 growth was accompanied by increased spontaneous erythroid differentiation as measured by benzidine staining [9].
• The impact of interindividual variation in NAT2 activity on benzidine urinary metabolites and urothelial DNA adducts in exposed workers [10].

Chemical compound and disease context of Benzydyna

• The carcinogen 4,4'-diaminobiphenyl (benzidine) has been compared in vitro with its terphenyl analogue 4,4''-diaminoterphenyl using the Salmonella reverse mutation assay and the BHK cell-transformation assay [11].
• Dapsone (4,4'-diaminodiphenyl sulfone) has a large clinical experience due to its antimicrobial effects against Mycobacterium leprae, the causative agent of leprosy, and is used clinically where inflammation mediated by neutrophils is perceived to play a role [12].
• A selection of 16 sulfonated azo dyes of both the monoazo type and diazo dyes based on benzidine, o-tolidine and o-dianisidine were assayed for mutagenicity in Salmonella typhimurium strains TA98 and TA100 employing both aerobic and anaerobic preincubation procedures [13].
• The metabolic basis of the differential activation of 4 benzidines--3,3'-dichlorobenzidine (DCB), benzidine (BZ), o-tolidine (TOL) and o-dianisidine (DIN)--to mutagens was examined in the Ames test, using Salmonella typhimurium TA98 [14].
• Mutagenicity of benzidine and benzidine-congener dyes and selected monoazo dyes in a modified Salmonella assay [15].

Biological context of Benzydyna

• This is shown by decrease in cell size, appearance of red and benzidine positive cells, and induced synthesis of four out of six adult globin chains [16].
• The hybrid cells were examined for globin gene expression by benzidine staining to detect cytoplasmic hemoglobin, and by molecular hybridization of cellular RNA to globin complementary DNA (cDNA) to detect globin messenger RNA (MRNA) [17].
• Embryos stain weakly with benzidine reagent, and yolk sac cells express globin RNAs, indicating globin gene activation in the absence of GATA-1 [18].
• Daily after plating, hemoglobin content was scored by benzidine staining, and growth was assessed by estimating the cell number per colony [19].
• The failure of metalloporphyrins other than hemin to stimulate the transient expression of a CAT reporter gene linked to an enhancer element containing a binding site for NF-E2 was correlated with their failure to induce benzidine-positive K562 cells and increase the steady-state level of gamma-globin mRNA [20].

Anatomical context of Benzydyna

• From 12 lymphocyte specimens studied thus far, significant interindividual variations were observed for 2-aminofluorene (62-fold), 7,12-dimethylbenz[a]anthracene (10-fold), benzidine (19-fold) and benzo[a]pyrene (18-fold) in their capacity to bind to the lymphocyte DNA [21].
• Larger colonies of over 1,000 benzidine-positive erythroid cells were developed from the fetal liver cells on the MSS cell layers after 6 days of incubation [22].
• No benzidine-positive cells or beta H1-globin mRNA expression was detected at the primitive streak or neural plate stage of development (E7.5) [23].
• The cooxidative metabolism of the urinary bladder carcinogen benzidine was examined using renal inner medullary microsomes [24].
• For several samples of urinary bladder epithelium, prostatic epithelium, colonic mucosa, and peripheral lung tissue, an arachidonic acid-dependent, microsomal-catalyzed activation of benzidine was observed; and the activity could be inhibited appreciably by indomethacin, a known inhibitor of PHS [25].

Associations of Benzydyna with other chemical compounds

• Isoelectric focusing of the CA-exposed cell lysate formed benzidine-positive foci in the positions of human adult Hb (HbA) and human fetal Hb (HbF) [26].
• Sodium butyrate was capable of markedly enhancing the number of benzidine-positive colonies (19.5 +/- 1/10(4) cells) formed, while the combination of sodium butyrate plus erythropoietin exerted a synergistic effect on erythropoietic colony formation (57 +/- 4/10(4) cells) [27].
• In comparison, human bladder and colon microsomes catalyzed the activation of benzidine greater than 4-aminobiphenyl, 2-amino-6-methyldipyrido[1,2-alpha:3',2'-d]imidazole, 2-naphthylamine greater than 2-amino-3-methylimidazo[4,5-f]quinoline, 3-amino-1-methyl-5H-pyrido[4,3-b]indole [25].
• With [3H]benzidine, p-aminobenzoic acid, a NAT1-specific substrate, increased the amount of benzidine and decreased the amount of N-acetylbenzidine produced, resulting in a decreased ratio of acetylated products [28].
• N-Hydroxy-N,N'-diacetylbenzidine (N-HO-DABZ) has been shown to be an in vitro metabolite of benzidine in several rodent species and may represent the proximate form of the carcinogen [29].

Gene context of Benzydyna

• Furthermore, in the presence of Epo, SCF (5 to 25 ng/mL) enhanced MB-02 proliferation in a dose-dependent manner, and increased the relative and absolute number of benzidine-positive cells generated [30].
• NAT2 slow acetylation and bladder cancer in workers exposed to benzidine [31].
• GSTP1 A1578G (Ile105Val) polymorphism in benzidine-exposed workers: an association with cytological grading of exfoliated urothelial cells [32].
• When K562 cells overexpressing CPOX were treated with delta-aminolevulinic acid (ALA), most became benzidine-positive without induction of the expression of CPOX or ferrochelatase, and the heme content was about twofold higher than that in ALA-treated control cells [33].
• Analysis of the TGF beta 1 effect on 10 different HEL-T-derived clones revealed that the number of benzidine-positive cells ranged from 12 to 70% after 5 days of continuous exposure [34].

Analytical, diagnostic and therapeutic context of Benzydyna

• After treatment with 20-30 micro M AMS for 4 days, the cultures contained between 80 and 90% benzidine-positive cells [35].
• Factors modulating benzidine carcinogenicity bioassay [2].
• Following culture and autoradiography, many lacZ-expressing benzidine-stained cells were observed in donor allantoises, but none contained silver grains above background [36].
• The mechanism(s) responsible for immunosuppression by benzidine, however, is probably not the same as that responsible for its direct carcinogenicity [3].
• Approximately 30% of the radioactivity recovered following HPLC of urine or bile was identified as unmetabolized benzidine [37].

References