The effect of tetrachlorohydroquinone on hexachlorobenzene‐induced porphyria in Japanese quail

Carpenter, Hillary M.; Harvey, Michael J.; Buhler, Donald R.

doi:10.1080/15287398509530637

Cited by 9 publications

(2 citation statements)

References 17 publications

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“…Oral administration of chemicals to Japanese quail by gelatin capsule is a convenient method for chronic dosing that has recently been success- fully used with HCB (Carpenter et al, 1981(Carpenter et al, , 1982. However, in the present studies, attempts to induce cytochrome P-450 and associated MFOs in birds by the oral administration of PB or BNF via gelatin capsules daily for up to 10 d were failures.…”

Section: Resultsmentioning

confidence: 71%

A comparison of the effects of hexachlorobenzene, β‐naphthoflavone, and phenobarbital on cytochrome p‐450 and mixed‐function oxidases in Japanese quail

Carpenter

Williams

Buhler

1985

Journal of Toxicology and Environmental Health

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Hexachlorobenzene (HCB), beta-naphthoflavone (BNF), or phenobarbital (PB) was administered to Japanese quail to determine their effects on hepatic porphyrin levels and drug-metabolizing enzymes. While HCB increased porphyrin levels, PB slightly reduced them, and BNF had no effect. HCB was an excellent inducer in quail, increasing the specific content of cytochrome P-450 to levels similar to those produced by BNF. Additional similarities between HCB- and BNF-treated quail included a comparable hypsochromic absorption shift in the CO-reduced difference spectra of cytochrome P-450 and similar effects on the activities of cytosolic glutathione S-transferase (GSH-t), biphenyl hydroxylase (BPH), and ethoxyresorufin O-deethylase (EROD). However, a differential response to HCB and BNF treatment was seen in the activities of hepatic NADPH-cytochrome P-450 reductase, epoxide hydrolase, GSH-t (microsomal), aryl hydrocarbon hydroxylase (AHH), and ethoxycoumarin O-deethylase (ECOD). The activities of NADPH-cytochrome P-450 reductase, AHH, and ECOD following treatment with HCB were similar to those found after dosing with PB. HCB caused a pattern of induction that was distinct from either BNF or PB and appeared to be a "mixed-type" inducer. The rapidity of the HCB-induced porphyrogenic response of Japanese quail, as compared to mammals, may provide unique advantages for making correlations between the in vivo metabolism of haloaromatic hydrocarbons and their effects on porphyrin metabolism.

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Section: Resultsmentioning

confidence: 71%

A comparison of the effects of hexachlorobenzene, β‐naphthoflavone, and phenobarbital on cytochrome p‐450 and mixed‐function oxidases in Japanese quail

Carpenter

Williams

Buhler

1985

Journal of Toxicology and Environmental Health

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“…e ALAS1 protein is the rate-limiting enzyme for haem synthesis in the liver by catalysing protoporphyrin production from ALA. en, protoporphyrin is converted into ferrous haem through the action of ferrochelatase (FECH) Evidence-Based Complementary and Alternative Medicine protein, and finally, haem is produced. e imbalance in porphyrin metabolism caused by ALAS1 has been proven to be related to liver damage caused by carbamazepine, tetrachlorohydroquinone, and hexachlorobenzene [36][37][38][39]. We analysed three SNPs in the ALAS1 gene (rs353556, rs3852071, and rs352169) but did not observe correlations with the susceptibility to ATDH.…”

Section: Discussionmentioning

confidence: 96%

Genetic and Functional Evaluation of the Role of FOXO1 in Antituberculosis Drug-Induced Hepatotoxicity

Zhang

Jiao

Song

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Background. The accumulation of the hepatotoxic substance protoporphyrin IX (PPIX) induced by aminolevulinate synthase 1 (ALAS1) activation is one of the important mechanisms of antituberculosis drug-induced hepatotoxicity (ATDH). Forkhead box protein O1 (FOXO1) may activate ALAS1 transcription. However, little is known about their roles in ATDH; we performed a study to determine the association between polymorphisms in the two genes and ATDH susceptibility. Then, we verified this possible association by cellular functional experiments. Materials and Methods. Tag single-nucleotide polymorphisms (TagSNPs) in the two genes were genotyped in 746 tuberculosis patients. The frequencies of the alleles, genotypes, genetic models, and haplotype distribution of the variants were compared between the case and control groups. L-02 cells and HepG2 cells were incubated with the indicated concentration of isoniazid (INH) and rifampicin (RIF) for the desired times, and then the expression levels of ALAS1 and FOXO1 mRNAs and proteins were detected. HepG2 cells were transiently transfected with FOXO1 siRNA to observe the effect of changes in the FOXO1 expression on the cell survival rate and ALAS1 expression. Results. The C allele at rs2755237 and the T allele at rs4435111 in the FOXO1 gene were associated with a decreased risk of ATDH. The expression of ALAS1 in both L-02 cells and HepG2 cells was increased by the coadministration of INH/RIF (600/200 μM) for 24 h. Although FOXO1 expression was reduced slightly by the same treatment, its content in the nucleus was significantly increased. However, the cell survival rate and ALAS1 expression level were not significantly altered by the downregulation of FOXO1 in HepG2 cells. Conclusions. Variants of the rs4435111 and rs2755237 loci in the FOXO1 gene were associated with susceptibility to ATDH. Coadministration of INH/RIF promoted the transfer of FOXO1 from the cytoplasm to the nucleus, but the functional significance of its nuclear translocation requires further verification.

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Association of Gene Polymorphisms and Serum Levels of ALAS1 with the Risk of Anti‐Tuberculosis Drug‐Induced Liver Injury

Han,

He,

Zhu

et al. 2024

The Journal of Clinical Pharma

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The accumulation of protoporphyrin IX in the liver caused by isoniazid and rifampicin through the disorder of heme biosynthesis was considered an important mechanism of anti‐tuberculosis drug‐induced liver injury (ATLI). Alanine synthase 1 (ALAS1) is a rate‐limiting enzyme in the process of heme synthesis. This study aimed to investigate the association between ALAS1 gene polymorphism, serum ALAS1 level, and the risk of ATLI. This study was a case‐control study including 58 ATLI cases and 192 controls. Four single nucleotide polymorphisms (SNPs) of the ALAS1 gene were selected for genotyping and serum ALAS1 concentrations were detected using ELISA kits. There was no significant difference in the genotype distribution of four SNPs between the ATLI cases and the controls under different genetic models. Patients carrying the GG genotype of SNP rs352163 in controls had higher baseline ALAS1 levels than those in ATLI cases (243.6 vs 290.2 ng/L, P = .034), and patients with baseline ALAS1 < 337.85 ng/L had a higher risk of ATLI than those with ALAS1 ≥ 337.85 ng/L (HR = 2.679, 95% CI: 1.360‐5.278, P = .004). Our findings indicated that the serum ALAS1 concentrations in the ATLI cases were lower than those in the controls, and the lower baseline ALAS1 levels can be associated with higher ATLI risk.

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The effect of tetrachlorohydroquinone on hexachlorobenzene‐induced porphyria in Japanese quail

Cited by 9 publications

References 17 publications

A comparison of the effects of hexachlorobenzene, β‐naphthoflavone, and phenobarbital on cytochrome p‐450 and mixed‐function oxidases in Japanese quail

A comparison of the effects of hexachlorobenzene, β‐naphthoflavone, and phenobarbital on cytochrome p‐450 and mixed‐function oxidases in Japanese quail

Genetic and Functional Evaluation of the Role of FOXO1 in Antituberculosis Drug-Induced Hepatotoxicity

Association of Gene Polymorphisms and Serum Levels of ALAS1 with the Risk of Anti‐Tuberculosis Drug‐Induced Liver Injury

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