[The role of smoking and metabolic enzyme polymorphisms in the organic solvent induced chronic encephalopathy].

OBJECTIVE

The organic solvents and other exogenous compounds of metabolic enzymes genetic variation may affect the risk of the toxic effect of organic solvents exposure. Therefore, this research we observed the glutathione transferase M1 and T1 (GSTM1, GSTT1) deletion mutation genotype, two kinds of microsomal epoxide hydrolase (mEPHX) genetic polymorphism, organic solvents exposure and smoking effection in chronic cases of toxic encephalopathy (CTE) correlation.

METHODS

The object was 115 patients who had a long history of organic solvents exposure, were divieded into two groups: CTE (n=83) , no CET (n=32) according to clinical diagnosis. DNA was isolated from patients in white blood cells through the multiple-polymerase chain reaction to determine the loss of GSTM1 and GSTT1 genotype. two kinds of mEPHX polymorphism were analysised through the PCR-RFLP (restriction fragment length polymorphism).

RESULTS

The relative risk has obviously improved when lack of GSTM1 genotypes to CTE (RR=2.35, 95% CI 2.35 0.96). in according to the patient's Smoking condition and classify genotype, patients lack of GSTM1 genotypes had a significantly higher risk CTE than GSTM1+genotype patients (RR=3.13, 95% CI 3.13 1.2) , both mEPHX polymorphisms had nothing to do with an increased risk of CTE.

CONCLUSION

The GSTM1 genotypes played an important role in the organic solvent induced the CTE of susceptibility.it was Influenced by the interaction between smoking at the same time.