Polymorphisms of the Xenobiotic-Metabolizing Enzymes CYP1A1 and NAT-2 in Systemic Sclerosis and Lupus Erythematosus

Schmiedeberg, Sherko von; Fritsche, Ellen; Rönnau, Andrea C.; Specker, Christof; Golka, Klaus; Richter-Hintz, Dagmar; Schuppe, H.‐C.; Lehmann, Percy; Ruzícka, T.; Esser, Charlotte; Abel, Josef; Gleichmann, Ernst

doi:10.1007/978-1-4615-4857-7_21

Cited by 51 publications

(24 citation statements)

References 15 publications

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“…The higher DDT and HCH levels in the SLE subjects compared to in control subjects from the same locale could be attributable to genetic defects in xenobiotic metabolizing enzymes such as CYP1A1, GSTM1 and NAT-2 (von Schmiedeberg et al, 1999;Horiuchi et al, 2009). Such defects would allow the pesticides to accumulate in the body.…”

Section: Discussionmentioning

confidence: 99%

Alterations in T-lymphocyte sub-set profiles and cytokine secretion by PBMC of systemic lupus erythematosus patients uponin vitroexposure to organochlorine pesticides

Dar

Das

Ramachandran

et al. 2012

Journal of Immunotoxicology

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Section: Discussionmentioning

confidence: 99%

Alterations in T-lymphocyte sub-set profiles and cytokine secretion by PBMC of systemic lupus erythematosus patients uponin vitroexposure to organochlorine pesticides

Dar

Das

Ramachandran

et al. 2012

Journal of Immunotoxicology

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“…One can imagine that this could be achieved by quick and efficient metabolic elimination of SCs or by preventing bioactivation altogether. It is noteworthy that the phenotype of slow acetylation by N-acetyltransferase, a phase-II enzyme, is more common in patients with drug-induced lupus caused by procainamid or hydralazine [10] [11]. Variant alleles of CYP1A1, which code for enzymes with higher activity, were found to protect against psoriasis [12].…”

Section: The Ahr -A Link Between Adversementioning

confidence: 97%

Small Chemicals, Bioactivation, and the Immune System – A Fragile Balance of i‐Tox and Benefits?

Esser

Jux

2009

Chemistry & Biodiversity

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Immunotoxicology concerns actions of chemicals which lead to adverse immune reactions. Current research challenges are the prediction of the immunotoxicologic risk potential of a chemical and a deeper mechanistic understanding of chemical-induced adverse immune reactions, to develop therapeutic or avoidance strategies. Small chemicals (SCs) can interfere with any cell type or function of the immune system. SCs are ubiquitous as food components, life-style products, or environmental pollutants. Besides their possible unspecific toxicity, they might form protein adducts, become part of recognized antigens, or they could be disruptors of immune signalling pathways. The incidence of autoimmune and allergic diseases has been rising over the last years, and evidence increases that SCs are important in this. Also, immunopharmacologists actively search for immunomodulating chemicals as urgently needed drugs. The aryl hydrocarbon receptor (AhR) is a SC-triggered transcription factor, and thus could link environmental signals to cellular responses. Recent research has shown a defined role for AhR in immunotoxicology. Here, we discuss concepts of SC immunotoxicity, and how AhR might be involved in adverse immune responses.

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“…N-acetyltransferase 2 (arylamine N-acetyltransferase) or NAT2 is polymorphic, metabolizes aromatic amines, and is involved in phase II metabolism of several compounds, such as caffeine and tobacco contents. This enzyme has been used in many studies relating acetylation capacity to disease, and a positive association between NAT2 activity and susceptibility to cancer (Ambrosone et al, 1996), Parkinson's disease (Agundez et al, 1998) and autoimmune diseases (von Schmiedeberg et al, 1999) has been reported. In particular, the mutations in the NAT2 isoenzyme are postulated to show a higher risk of cancers.…”

Section: Introductionmentioning

confidence: 99%

Genetic polymorphisms of EGF 5'-UTR and NAT2 857G/A associated with glioma in a case control study of Malaysian patients

Muthusamy

Lian²,

Vairavan³

et al. 2012

Genet. Mol. Res.

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ABSTRACT. Studies of genetic mutations that have been used in predicting glioma prognosis have revealed a complex relationship between clinical and genetic factors. Epidermal growth factor (EGF) and the NAT2 gene play a central role in carcinogenesis. An adenine (A) to guanine (G) single nucleotide polymorphism at position 61 in the 5'-untranslated region (5'-UTR) of the EGF gene has been found to be associated with levels of EGF production, and the mutations in the NAT2 gene have been postulated as a risk factor for cancer. We investigated EGF and the NAT2 gene in 13 glioma tissue samples and 12 normal controls. In the EGF 5'-UTR 61G polymorphism, the heterozygote GA was the most common genotype in the glioma patients. In the NAT2 polymorphism at nucleotide position 857G/A, the G allele and the GG genotype were the most prevalent forms in both the glioma and normal samples. We did not find any homozygous AA genotypes in the glioma patients. Based on this preliminary evidence, the EGF 5'-UTR at position 61 and the NAT2 SNP at position 857 polymorphisms are associated with increased risk for glioma.

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Polymorphisms of the Xenobiotic-Metabolizing Enzymes CYP1A1 and NAT-2 in Systemic Sclerosis and Lupus Erythematosus

Cited by 51 publications

References 15 publications

Alterations in T-lymphocyte sub-set profiles and cytokine secretion by PBMC of systemic lupus erythematosus patients uponin vitroexposure to organochlorine pesticides

Alterations in T-lymphocyte sub-set profiles and cytokine secretion by PBMC of systemic lupus erythematosus patients uponin vitroexposure to organochlorine pesticides

Small Chemicals, Bioactivation, and the Immune System – A Fragile Balance of i‐Tox and Benefits?

Genetic polymorphisms of EGF 5'-UTR and NAT2 857G/A associated with glioma in a case control study of Malaysian patients

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