Glutathione S-transferase M1 and GST T1 genetic polymorphisms and Raynaud’s phenomenon in French vinyl chloride monomer-exposed workers

Fontana, Luc; Marion, Marie‐Jeanne; Ughetto, Sylvie; Catilina, P.

doi:10.1007/s10038-006-0038-9

Cited by 14 publications

(12 citation statements)

References 34 publications

(59 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, studies of RP patients that were exposed to vinyl chloride monomer (VCM) suggest that the interaction between a certain genetic background and environmental conditions may play a role in increasing the onset of RP in VCM-exposed individuals (Fontana et al, 2006). In 2006, Fontana et al (2006) investigated whether there is an association between polymorphisms in glutathione S -transferase M1 and T1 genes and RP patients exposed to VCM (Fontana et al, 2006).…”

Section: Rp and Genetic Backgroundmentioning

confidence: 99%

“…In 2006, Fontana et al (2006) investigated whether there is an association between polymorphisms in glutathione S -transferase M1 and T1 genes and RP patients exposed to VCM (Fontana et al, 2006). The results showed that the combination of positive genotypes for both genes may increase susceptibility to RP (Fontana et al, 2006).…”

Section: Rp and Genetic Backgroundmentioning

confidence: 99%

See 1 more Smart Citation

Raynaud’s Phenomenon: A Brief Review of the Underlying Mechanisms

et al. 2016

View full text Add to dashboard Cite

Raynaud’s phenomenon (RP) is characterized by exaggerated cold-induced vasoconstriction. This augmented vasoconstriction occurs by virtue of a reflex response to cooling via the sympathetic nervous system as well as by local activation of α2C adrenoceptors (α2C-AR). In a cold-initiated, mitochondrion-mediated mechanism involving reactive oxygen species and the Rho/ROCK pathway, cytoskeletal rearrangement in vascular smooth muscle cells orchestrates the translocation of α2C-AR to the cell membrane, where this receptor readily interacts with its ligand. Different parameters are involved in this spatial and functional rescue of α2C-AR. Of notable relevance is the female hormone, 17β-estradiol, or estrogen. This is consistent with the high prevalence of RP in premenopausal women compared to age-matched males. In addition to dissecting the role of these various players, the contribution of pollution as well as genetic background to the onset and prevalence of RP are also discussed. Different therapeutic approaches employed as treatment modalities for this disease are also highlighted and analyzed. The lack of an appropriate animal model for RP mandates that more efforts be undertaken in order to better understand and eventually treat this disease. Although several lines of treatment are utilized, it is important to note that precaution is often effective in reducing severity or frequency of RP attacks.

show abstract

Section: Rp and Genetic Backgroundmentioning

confidence: 99%

Section: Rp and Genetic Backgroundmentioning

confidence: 99%

Raynaud’s Phenomenon: A Brief Review of the Underlying Mechanisms

et al. 2016

View full text Add to dashboard Cite

show abstract

“…The vascular endothelial toxicity of vinyl chloride has been shown by angiographic studies of arteries in the hand and by capillaroscopy [104,105]. The prevalence of RP in vinyl chloride workers ranges from 6 to 33% [106]. In 1980 a prospective exposed/non-exposed cohort study showed a strong association between vinyl chloride exposure and RP (P<0.006) [107].…”

Section: Endothelium Damage And/or Neurotoxicitymentioning

confidence: 99%

Drug‐induced Raynaud's phenomenon: beyond β‐adrenoceptor blockers

Khouri

Blaise

Carpentier

et al. 2016

Brit J Clinical Pharma

View full text Add to dashboard Cite

AIMDrug-induced Raynaud's phenomenon (RP) has long been associated with the use of different drugs, including cancer chemotherapy or β-adrenoceptor blockers. However, sources report extremely variable prevalence and the level of evidence for each class is heterogeneous. Moreover, new signals are emerging from case reports and small series. Our objective was therefore to review available evidence about this adverse drug effect and to propose a mechanistic approach of drug-induced RP. METHODSA systematic review of English and French language articles was performed through Medline (1946Medline ( -2015 and Embase (1974Embase ( -2015. Further relevant papers were identified from the reference lists of retrieved articles. RESULTSWe identified 12 classes of drugs responsible for RP, with a variety of underlying mechanisms such as increased sympathetic activation, endothelial dysfunction, neurotoxicity or decreased red blood cell deformability. Cisplatin and bleomycin were associated with the highest risk, followed by β-adrenoceptor blockers. Recent data suggest a possible involvement of tyrosine kinase inhibitors (TKI), through an unknown mechanism. CONCLUSIONDrug-induced RP is a probably underestimated adverse drug event, with limited available evidence regarding its prevalence. Although rare, serious complications like critical digital ischaemia have been reported. When these treatments are started in patients with a history of RP, careful monitoring must be made and, if possible, alternative therapies that do not alter peripheral blood flow should be considered. IntroductionRaynaud's phenomenon (RP) is characterized by transient ischaemia of the extremities in response to environmental stress or emotions [1]. It typically manifests as changes to the fingers, with pallor (vasospasm and decreased blood flow), cyanosis (deoxygenation of the static venous blood) and rubor (reperfusion), often accompanied by pain. RP can be primary (i.e. idiopathic) or secondary to an underlying cause. In both cases, abnormalities of the cutaneous microcirculation are primarily involved in the pathophysiology of RP [2]. The prevalence of RP in the general population varies between 0.5 and 19%, with major geographic variability [3][4][5][6]. While primary RP is the most frequent form (80-90%) [7], RP may also be secondary to various auto-immune diseases (such as systemic sclerosis (SSc), systemic lupus erythematosus, vasculitis, etc.), or other systemic diseases [1]. Several drugs with peripheral vascular effects leading to decreased microvascular perfusion may induce or aggravate RP. Drug-induced RP probably goes unrecognized because of the limited knowledge of this side effect. British Journal of Clinical PharmacologyLiterature reviews and textbooks usually have comprehensively reviewed drugs that have long been known to be responsible for RP [8]. However, new signals are emerging from numerous case reports. Yet, to our knowledge, no systematic review has been performed and little is known about the prevalence and the level of evidence ...

show abstract

“…Many studies have investigated the effect of genetic polymorphisms of genes involved in metabolism (CYP2E1, GST, mEH, ALDH2) and DNA repair (XRCC1, XPD; refs. 6,[9][10][11][12][13][14][15]. To the best of our knowledge, however, no studies have been conducted on the effect of genetic polymorphisms of genes involved in cell cycle control.…”

Section: Introductionmentioning

confidence: 99%

Genetic Polymorphisms, Messenger RNA Expression of p53, p21, and CCND1, and Possible Links with Chromosomal Aberrations in Chinese Vinyl Chloride–Exposed Workers

Qiu

Wang

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

View full text Add to dashboard Cite

This study explores the relationship between genetic polymorphisms of p53, p21, and CCND1, and the susceptibility of chromosomal damage induced by vinyl chloride monomer (CH 2 = CHCl, VCM). Besides gene polymorphisms, we detected the mRNA expression of p53, p21, and CCND1 in VCM-exposed workers and in a control group. One hundred and eighty-three workers occupationally exposed to VCM were investigated. Chromosome damage in peripheral lymphocyte was measured by cytokinesis-block micronucleus assay. The PCR-restriction fragment length polymorphism technique was applied to detect polymorphisms of p53, p21 (exon 2 and exon 3), and CCND1 genes (exon 4). The quantity of gene mRNA expression was detected by realtime PCR (SYBR Green I). Taking into account the effects of genetic polymorphisms, as well as demographic and habitual factors, Poisson regression analysis showed that the risk of chromosomal damage induced by VCM for individuals carrying the p53 intron 6 heterozygous and mutant homozygous genotype was 1.23 times larger (90% confidence interval, 1.01-1.51 P = 0.0814), compared with those carrying wild-type homozygous genotypes. The p53 exon 4, intron 3, and intron 6 haplotype pairs of MMM/WWW (M, mutation allele; W, wild allele), and MWM/WWW were associated with increased frequencies of micronuclei. The p53 mRNA expression of VCM-exposed workers was significantly lower than that of nonexposed workers, but p21 mRNA expression in VCM-exposed workers was significantly higher than that of nonexposed workers. Our findings suggest that the p53 intron 6 polymorphism is one of the factors that potentially influence the frequency of micronuclei induced by VCM. (Cancer Epidemiol Biomarkers Prev 2008;17(10):2578 -84)

show abstract

Glutathione S-transferase M1 and GST T1 genetic polymorphisms and Raynaud’s phenomenon in French vinyl chloride monomer-exposed workers

Cited by 14 publications

References 34 publications

Raynaud’s Phenomenon: A Brief Review of the Underlying Mechanisms

Raynaud’s Phenomenon: A Brief Review of the Underlying Mechanisms

Drug‐induced Raynaud's phenomenon: beyond β‐adrenoceptor blockers

Genetic Polymorphisms, Messenger RNA Expression of p53, p21, and CCND1, and Possible Links with Chromosomal Aberrations in Chinese Vinyl Chloride–Exposed Workers

Contact Info

Product

Resources

About