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PubMed1989

Pretreatment with mixed-function oxidase inducers increases the sensitivity of the hepatocyte/DNA repair assay.

A recent National Toxicology Program evaluation indicates that the rat hepatocyte/DNA repair assay has a high false-negative rate and that it is insensitive to some genotoxic hepatocarcinogens as well as other species and organ-specific carcinogens. In this study, we examined whether the sensitivity of the hepatocyte/DNA repair assay might be increased through animal pretreatment with various hepatic mixed-function oxidase inducers, i.e., Aroclor 1254, phenobarbital, and 3,3',4,4'-tetrachloroazobenzene (TCAB). The effects on unscheduled DNA synthesis (UDS), a measure of DNA damage and repair, were studied in cultures exposed to known and/or potential carcinogens that had been evaluated as negative or questionable or that produced conflicting results with hepatocytes isolated from uninduced animals. 4,4'-Oxydianiline, 1-nitropyrene, and TCAB produced concentration-dependent increases in UDS in hepatocytes from rats pretreated with Aroclor 1254. 4,4'-Oxydianiline and TCAB also induced a dose-dependent increase in DNA repair in hepatocytes from rats pretreated with phenobarbital, whereas 1-nitropyrene was negative. 4,4'-Methylenedianiline produced a marginal response, and 3,3',4,4'-tetrachloroazoxybenzene (TCAOB) was negative in Aroclor- and phenobarbital-induced hepatocytes; however, TCAOB, as well as TCAB, produced concentration-dependent increases in UDS in TCAB-induced hepatocytes. These data indicate that the limited sensitivity to chemical carcinogens displayed by the hepatocyte/DNA repair assay may be increased by using hepatocytes isolated from animals exposed to hepatic mixed-function oxidase inducers.

Animals↗

PubMed1990

Metabolism of the arylamide herbicide propanil. II. Effects of propanil and its derivatives on hepatic microsomal drug-metabolizing enzymes in the rat.

Propanil (3,4-dichloropropionanilide) is an arylamide herbicide that has been reported to be contaminated with the cytochrome P450 enzyme inducers 3,3',4,4'-tetrachloroazobenzene (TCAB) and 3,3',4,4'-tetrachloroazoxybenzene (TCAOB), which are structural analogs of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). We determined if treatment of rats with TCAB, TCAOB, propanil, 3,4-dichloroaniline, TCDD, or phenobarbital induced the hepatic microsomal metabolism of propanil and 3,4-dichloroaniline. Acylamidase-catalyzed hydrolysis of propanil to 3,4-dichloroaniline was not induced by any of the pretreatments; however, hydroxylation of propanil at the 2'-position was induced by TCDD, TCAB, TCAOB, propanil, and 3,4-dichloroaniline pretreatments. Ring- and N-hydroxylations of 3,4-dichloroaniline were induced by TCDD, TCAB, TCAOB, and 3,4-dichloroaniline pretreatments. Microsomal 7-ethoxyresorufin-O-deethylase (EROD) and 7-benzoxyresorufin-O-dealkylase (BROD) activities and electrophoretic mobility of microsomal proteins suggested that cytochromes P450c and P450d were induced by TCAB and TCAOB pretreatment. EROD, BROD, and 7-pentoxyresorufin-O-dealkylase activities were slightly increased in microsomes from propanil- and 3,4-dichloroaniline-pretreated rats, which suggests that these compounds may be weak inducers of cytochrome P450 isozymes.

Anilides↗

PubMed1977

3,4,3',4'-tetrachloroazobenzene: a potential environmental toxicant.

3,4,3',4'-tetrachloroazobenzene (TCAB), a potential environmental toxicant formed in the industrial manufacturing and the microbial degradation of chloroanilide herbicides, has been prepared in 87% yield by an improved procedure. In vitro experiments with C3H/10T1/2 cells have shown that TCAB is toxic to mammalian cells, which may be correlated with observable cytological changes. TCAB has also been found to be weakly mutagenic by the Salmonella/microsome test. In addition, C3H/10T1/2 cells are transformed following a ten day incubation with TCAB. These data suggest the potential health hazard associated with the environmental occurrence of TCAB.

Animals↗

PubMed2023

Teicoplanin associated gene tcaA inactivation increases persister cell formation in Staphylococcus aureus.

Staphylococcus aureus is part of normal human flora and is widely associated with hospital-acquired bacteremia. S. aureus has shown a diverse array of resistance to environmental stresses and antibiotics. Methicillin-resistant S. aureus (MRSA) is on the high priority list of new antibiotics discovery and glycopeptides are considered the last drug of choice against MRSA. S. aureus has developed resistance against glycopeptides and the emergence of vancomycin-intermediate-resistant, vancomycin-resistant, and teicoplanin-resistant strains is globally reported. Teicoplanin-associated genes tcaR-tcaA-tcaB (tcaRAB) is known as the S. aureus glycopeptide resistance operon that is associated with glycopeptide resistance. Here, for the first time, the role of tcaRAB in S. aureus persister cells formation, and ΔtcaA dependent persisters' ability to resuscitate the bacterial population was explored. We recovered a clinical strain of MRSA from a COVID-19 patient which showed a high level of resistance to teicoplanin, vancomycin, and methicillin. Whole genome RNA sequencing revealed that the tcaRAB operon expression was altered followed by high expression of glyS and sgtB. The RNA-seq data revealed a significant decrease in tcaA (p = 0.008) and tcaB (p = 0.04) expression while tcaR was not significantly altered. We knocked down tcaA, tcaB, and tcaR using CRISPR-dCas9 and the results showed that when tcaA was suppressed by dCas9, a significant increase was witnessed in persister cells while tcaB suppression did not induce persistence. The results were further evaluated by creating a tcaA mutant that showed ΔtcaA formed a significant increase in persisters in comparison to the wild type. Based on our findings, we concluded that tcaA is the gene that increases persister cells and glycopeptide resistance and could be a potential therapeutic target in S. aureus.

MRSA↗

PubMedDate not supplied

Levels of 3,3',4,4'-tetrachloroazobenzene in diuron and linuron herbicide formulations.

Levels of 3,3',4,4'-tetrachloroazobenzene (TCAB) were determined by capillary gas chromatography (GC) with electron-capture detection (ECD) in 25 samples of diuron and linuron formulations obtained from the Canadian market. Acidic aqueous methanol was used to retain urea herbicide and the neutral TCAB was allowed to partition into hexane. Silica gel was used for cleanup of the hexane extract, followed by GC/ECD determination. Recovery data obtained at 4 different spiking levels (i.e., 0.3, 0.1, 1.0, and 5.0 ppm) in linuron averaged 93, 86, 85, and 97%, respectively. For diuron, spiking was done at 0.5, 1.0, and 5.0 ppm levels and the corresponding average percent recoveries were 95, 101, and 104. The TCAB contamination level observed in diuron on a 100% active ingredient basis ranged from 0.15 to 3.38 ppm, whereas in linuron, it varied from 0.91 to 10.28 ppm.

Azo Compounds↗

PubMed1979

Induction of hepatic microsomal cytochrome P-448 by 3,3',4,4'-tetrachloroazobenzene and the corresponding azoxy and hydrazo analogs.

3,3',4,4'-Tetrachlorazobenzene (TCAB) has been found to pose occupational health hazards among chemical workers as a consequence of its contamination in commercially important herbicides. The induction of hepatic microsomal cytochrome levels in male rats treated with TCAB or its azoxy and hydrazo analogs were examined in several short-term experiments. Five daily consecutive administrations of TCAB or 3,3',4,4'-tetrachloroazoxybenzene (TCAOB) at doses of 25 mg/kg/day yielded maximal stimulation of cytochrome levels. Both compounds induced cytochrome P-450 with absorption maxima (reduced, CO complex) at 448 nm to 2.7 times control levels. In contrast, cytochrome P-448 levels were enhanced less than twofold relative to controls in animals treated with 3,3',4,4'-tetarchlorohydrazobenzene (TCHB) under identical conditions. Cytochrome inductions arising from these chemicals are dose dependent. Parallel increase of the liver to body weight ratios was also observed in these studies. Further experiments using different regimens indicated TCAOB as being the most potent and persistent inducer among these three analogs. A twofold enhancement of cytochome P-448 levels was observed 14 days after a single ip injection of TCAOB at doses as low as 10 mg/kg.

Animals↗

PubMed1988

Evaluation of propanil and its N-oxidized derivatives for genotoxicity in the Salmonella typhimurium reversion, Chinese hamster ovary/hypoxanthine guanine phosphoribosyl transferase, and rat hepatocyte/DNA repair assays.

Since the herbicide propanil (3,4-dichloropropionanilide) is an aromatic amide and many other aromatic amides are genotoxic via N-hydroxy (N-OH) metabolites, N-oxidized derivatives of propanil and 3,4-dichloroaniline were synthesized and tested for genotoxicity. Propanil 3,4-dichloroaniline, and their N-OH derivatives were not mutagenic in the Salmonella typhimurium reversion assay using tester strains TA97, TA98, TA100, and TA104, in both the presence and absence of exogenous metabolic activation (S9). In addition, the test compounds were not mutagenic in the Chinese hamster ovary/hypoxanthine guanine phosphoribosyl transferase (CHO/HGPRT) assay, in both the presence and absence of S9. 3,3',4,4'-Tetrachloroazobenzene (TCAB) and its azoxy derivative (TCAOB), which are synthetic contaminants and/or degradation products of propanil, were also inactive in the S. typhimurium reversion and CHO/HGPRT assays (+/- S9). Unscheduled DNA synthesis (UDS) assays were performed to determine if propanil derivatives were able to induce DNA damage in primary rat hepatocytes. Although TCAB was the only derivative tested which induced an elevation in DNA repair, the extent was not statistically significant. Hepatocyte toxicity, as measured by the release of lactate dehydrogenase 24 hr after exposure, was induced by all the test compounds in a concentration-dependent manner. Incubations of [14C]N-OH-3,4-dichloroaniline with DNA in vitro resulted in only a low level of binding that was not affected by pH. This observation may partially explained the lack of mutagenicity observed in genotoxicity assays with propanil derivatives.

Anilides↗

PubMed1976

3,4,3',4'-Tetrachloro azoxybenzene and azobenzene: potent inducers of aryl hydrocarbon hydroxylase.

Two unwanted contaminants, 3,4,3',4'-tetrachloroazoxybenzene (TCAOB) and 3,4,3',4'-tetrachloroazobenzene (TCAB), formed in the commercial synthesis of 3,4-dichloroaniline or of herbicides made from 3,4-dichloroaniline, were responsible for three outbreaks of acne among chemical workers. TCAOB and TCAB are approximately isosteric to 2,3,7,8-tetrachlorodibenzo-p-dioxin and 2,3,7,8-tetrachlorodibenzofuran, two well-known contaminants that cause acne. All four of these agents are potent inducers of hepatic aryl hydrocarbon hydroxylase activity and compete for stereospecific binding sites in the hepatic cytosol, which are thought to be the receptor sites for the induction of this enzyme. Among the chlorinated azoxy and azobenzenes, the potency of a congener to induce aryl hydrocarbon hydroxylase activity correlates with its binding affinity for the hepatic cytosol specific binding sites and its capacity to induce acne; this relation between structure and activity parallels that observed for the chlorinated dibenzo-p-dioxins and dibenzofurans.

Acne Vulgaris↗

PubMed1977

Chloracne from manufacture of a new herbicide.

Forty-one chemical company workers had chloracne as a result of exposure to 3,4,3',4'-tetrachloroazoxybenzene (TCAB), an extraneous intermediate produced during the manufacture of a new herbicide. There was no laboratory evidence of significant hepatotoxicity or porphyria during the short time the herbicide was produced. An acnegenic when applied to the rabbit ear, TCAB is also a potent inducer of the microsomal enzyme aryl hydrocarbon hydroxylase. Prevention of chlorance is a difficult industrial engineering task and treatment of the disease is even more perplexing.

Acne Vulgaris↗

PubMed1985

Delayed wasting syndrome and alterations of liver gluconeogenic enzymes in rats exposed to the TCDD congener 3,3', 4,4'-tetrachloroazoxybenzene.

A delayed wasting syndrome similar to that induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was observed in male Sprague-Dawley rats exposed to 3,3', 4,4'-tetrachloroazoxybenzene (TCAOB) and 3,3',4,4'-tetrachloroazobenzene (TCAB). After a slow growth period, all treatment animals (25 mg/kg, i.p., 2 doses per week) exhibited a starvation-like syndrome characterized by reduced food intake, dramatic loss of body weight and subsequent death. Although the growth of all major organs in the treatment animals was affected, the thymus appeared severely atrophied. The growth kinetics during the earlier phase were further analyzed using serially-killed rats receiving TCAOB. In addition, TCAOB was found to markedly depress the specific activity (mumol/min/g wet liver) of glucose-6-phosphatase, fructose-1,6-bisphosphatase, phosphoenolpyruvate carboxykinase, and pyruvate kinase in the liver. Significant changes in the levels of cytochrome P-450, glutamic-pyruvic transaminase and malic enzyme in the liver were also observed.

Animals↗

PubMed1979

Induction of unscheduled DNA synthesis in suspensions of rat hepatocytes by an environmental toxicant, 3,3'4,4'-tetrachloroazobenzene.

Unscheduled DNA synthesis was induced by 3,3'4,4'-tetrachloroazobenzene (TCAB)) in freshly isolated suspensions of rat hepatocytes. A dose-dependent response was demonstrated. Hepatocellular DNA was obtained after the chloroform-isoamyl alchohol-phenol extraction of the isolated nuclei. The induction of unscheduled DNA synthesis was measured by the incorporation of [3H]-thymidine in the presence of hydroxyurea as determined by the scintillation counting assay. DNA repair data obtained in this study on benzo[a]pyrene and methyl methanesulfonate are comparable to a previous report using primary cultures of hepatocytes and cesium chloride gradients. Hence, the present method offers promise as a rapid and sensitive screen for chemical carcinogens.

Animals↗

PubMed1989

Measurement and clinical significance of thyroid microsomal and thyroglobulin antibodies by enzyme-linked immunosorbent assay.

Using the thyroid microsomal antigen(TMAg) prepared by affinity chromatography gel filtration method of sufficient purity, we measured the TM antibody (TMAb) level by an enzyme-linked immunosorbent assay (ELISA) in 103 normal persons and 183 patients with various thyroid disorders (Hashimoto's thyroiditis, Graves' disease, hypothyroidism, subacute thyroiditis, thyroid cancer, thyroid adenoma and simple goiter). The thyroglobulin antibody (TCAb). T3 and T4 were also measured at the same time. Based on the measurement of TMAb and TGAb of the thyroid diseases and analysis of their incidences and titer, our data strongly support that ELISA using purified TM and TG is a very useful and promising method for diagnosis and distinguishing autoimmune from non-autoimmune thyroid disease, and also can be employed in monitoring the development and studying the pathogenesis of the disease. We found that there is a negative correlation between TMAb titer and T3, T4 values (P less than 0.01) which has not been reported before in the literature. According to the result of the study, we suggest an immunological classification of thyroid diseases.

Adult↗