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Results for “Cytochrome P-450 CYP1A1”

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PubMed1979

Induction of the hepatic microsomal and nuclear cytochrome P-450 system by hexachlorobenzene, pentachlorophenol and trichlorophenol.

The application of hexachlorobenzene (HCB), pentachlorophenol (PCP) and 2,4,5-trichlorophenol (TCP) to female rats led to an induction of both the microsomal and the nuclear cytochrome P-450 system in the liver. The increase of th mixed-function hydroxylase activities examined (7-ethoxycoumarin deethylase, 7-ethoxyresorufin deethylase, NADPH-dependent cytochrome c reductase, aminopyrine demethylase, benzpyrene hydroxylase) did not correlate strictly with the cytochrome P-450 content. Depending on the inducers and the substrates used, the content and the activity of the cytochrome P-450 were essentially smaller in the nuclei than in the microsomes. It was striking that in the nuclei those activities (benzpyrene hydroxylase, 7-ethoxyresorufin deethylase, 7-ethoxycoumarin deethylase) were preferably induced which can be attributed to the methyl-cholanthrene-induced form of the cytochrome P-450 (cytochrome P-448). These results suggest, also in the light of findings of other authors, the induction of different species of cytochrome P-450 in the nuclei and microsomes.

7-Alkoxycoumarin O-Dealkylase↗

PubMed2025

Antiepileptic drugs carbamazepine and valproic acid mediate transcriptional activation of CYP1A1 via aryl hydrocarbon receptor and regulation of estrogen metabolism.

Cytochrome P450 1A1 (CYP1A1) actively catalyzes estrogen hydroxylation reactions and maintains the levels of neuroactive steroid estradiol. The widely prescribed first-line anti-epileptic drugs (AEDs) are considered to be a potent inducer of CYP1A1 and have also been observed to affect serum estradiol and calcium levels in patients with epilepsy. However, the ability of AEDs to interfere with CYP enzyme function and estrogen disposition is a relatively unexplored area. Here we investigate the effect of widely prescribed AEDs (carbamazepine and valproic acid) on CYP1A1 regulation and the levels of estradiol and calcium in cell supernatants of hepatocellular, HepG2, and neuronal, SH-SY5Y cells. We observed that both the AEDs significantly increased CYP1A1 expression and enzyme activity, which was accompanied by a decrease in estradiol and calcium levels in HepG2 cells. This induction of CYP1A1 mRNA and protein was fully prevented by aryl hydrocarbon receptor (AHR) knockdown and StemRegenin 1 (SR1) antagonism. Notably, the AEDs did not affect the AHR expression but regulated its nuclear translocation, potentially driving the transcriptional upregulation of CYP1A1. Furthermore, the knockdown of CYP1A1 in HepG2 cells elucidated a marked increase in estradiol and calcium levels. Later, this increase subsided upon AED exposure. Lastly, we observed a similar trend in estradiol and calcium alterations in SH-SY5Y cells on AED exposure, speculating the involvement of CYP1A1 induction via AEDs at neuronal sites. This work demonstrates that AEDs mediate the upregulation of CYP1A1 via an AHR-dependent mechanism and influence estrogen and calcium homeostasis.

Humans↗

PubMed2026

A systematic review and network meta-analysis of single nucleotide polymorphisms associated with oral submucous fibrosis risk.

BACKGROUND: Oral submucous fibrosis (OSF) is a chronic and insidious oral disease characterized by hyalinization of the subepithelial connective tissue and progressive fibrosis of the oral submucosa. It is a precancerous condition of oral squamous cell carcinoma. Studies have demonstrated that single nucleotide polymorphisms (SNPs) are closely associated with susceptibility to OSF. This study aims to comprehensively evaluate the association between SNPs and OSF risk and to rank the strength of the association between different genetic models and OSF susceptibility. METHODS: Literature related to OSF was comprehensively searched from PubMed, Web of Science, Embase, Cochrane Library, CNKI, and Wangfang databases up to July 2025. Full-text case-control studies with patients diagnosed with OSF were included. Quality assessment was performed to evaluate the risk of bias. RevMan 5.4, GeMTC 0.14.3, and STATA 17.0 were used for the pairwise and Bayesian network meta-analysis. RESULTS: A total of 24 studies with 2545 cases and 3772 controls, covering 13 SNPs in 11 genes, were included in our meta-analysis. We found that CYP1A1 rs4646903:T>C, CYP1A1 rs1048943:A>G, GSTT1 null genotype, GSTM1 null genotype, and XRCC3 rs861539:C>T were associated with an increased risk of OSF, while MMP2 rs243865:C>T and MMP3 rs3025058: 5A>6A were associated with a decreased risk of OSF. Further Bayesian network meta-analysis indicated the top 5 genetic models with the highest association with OSF risk in network group 1 were the dominant model, homozygous model, allelic model, and recessive model of CYP1A1 rs1048943:A>G (ranked 1-4), and the heterozygous/dominant model of CYP1A1 rs4646903:T>C (both ranked 5). While the allelic models of XRCC3 rs861539:C>T and MMP3 rs3025058: 5A>6A ranked first for predicting OSF in group 2 and group 3, respectively. CONCLUSION: Some specific SNPs are significantly related to the risk of OSF. Among them, the dominant model of CYP1A1 rs1048943:A>G may be the most strongly associated genetic model with OSF risk. Future large-sample, well-designed studies with detailed genotype data are needed to validate the roles of these SNPs in OSF risk.

Humans↗

PubMed1979

Catecholestrogen synthesis and metabolism by human breast tumors in vitro.

The activities of enzymes which synthesize and metabolize catecholestrogens were studied in biopsy samples of human breast neoplasms. Estrogen 2-hydroxylase, a cytochrome P-450-dependent enzyme, was present in both benign and malignant neoplasms but not in normal breast tissue. Catechol O-methyltransferase activity was present in all samples examined and was significantly higher in malignant tumors [549 +/- 31 (S.E.) pmol/20 min/mg protein] than in benign neoplasms (226 +/- 41 pmol/20 min/mg protein) or in normal breast tissue (133 +/- 28 pmol/20 min/mg protein). There was no correlation, however, between estrogen 2-hydroxylase and catechol O-methyltransferase activities. The enzymes responsible for the synthesis and metabolism of catecholestrogens are present in some breast tumor specimens, suggesting that in such tissues these metabolites may be formed in vivo.

Breast↗