OBJECTIVETo study the cellular and molecular mechanism of gasoline-induced adverse effects on skin, particularly on keratinocyte and fibroblast in vitro.

METHODSThe primary cell culture of keratinocyte and fibroblast were treated with 0, 0.001%, 0.01%, 0.1% and 1.0% gasoline, respectively. (3)H-thymidine ((3)H-TdR), (3)H-leucine ((3)H-Leu), (3)H-proline ((3)H-Pro) and (14)C-linoleic acid incorporation tests were applied to elucidate their capacity of synthesizing DNA, protein and sebum.

RESULTSThe incorporation of (3)H-TdR in keratinocyte and (3)H-TdR and (3)H-Pro in fibroblast inhibited significantly after exposure to 0.01% gasoline (P < 0.05), with inhibition rates 68.5%, 45.1% and 40.6% for (3)H-TdR in keratinocyte, and (3)H-TdR and (3)H-Pro in fibroblast, respectively. Significant depression in incorporation of (3)H-Leu and (14)C-linoleic acid in keratinocyte were found even in the group treated with 0.001% gasoline (P < 0.05), with inhibition rates of 20.2% and 41.2%, respectively.

CONCLUSIONSSolvent gasoline has certain toxic effect on keratinocyte and fibroblast, intervening their normal metabolic and physiological process and affecting their ability of synthesizing DNA, protein and sebum, and their physiological functions, which could be one of the mechanisms causing skin damage by gasoline. The results also indicated that keratinocyte was more susceptible to gasoline than fibroblast.

Animals ; Cells, Cultured ; DNA ; biosynthesis ; genetics ; Dose-Response Relationship, Drug ; Fibroblasts ; cytology ; drug effects ; metabolism ; Gasoline ; toxicity ; Keratinocytes ; cytology ; drug effects ; metabolism ; Proteins ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley ; Sebum ; drug effects ; metabolism

OBJECTIVETo explore the relation between genetic polymorphisms of NQO1, GSTT1 and risks of chronic benzene poisoning (BP).

METHODSA case-control study was conducted. 152 BP patients and 152 workers occupationally exposed to benzene without poisoning manifestations were investigated. Polymerase chain reaction (PCR), denaturing high-performance liquid chromatography(DHPLC) and sequencing were used to detect the single nucleotide polymorphisms(SNPs) of the promoter and complete coding-region of NQO1 gene. Multiple PCR was used to detect GSTT1 genotype.

RESULTSIn smoking population, there was 7.73-fold (95% CI: 1.71-34.97, P = 0.010) of risk in BP subjects carrying NQO1c. 609 T/T genotype, compared with those carrying C/C and C/T. genotype. In drinking population, the individuals carrying the 6th extron of NQO1c. 609 T/T homozygote genotype had a 11.00-fold(95% CI: 1.89-63.83, P = 0.005) risk of BP compared to those with NQO1c. 609 C/T and C/C genotypes.

CONCLUSIONThe subjects carrying NQO1c. 609 T/T genotype and together with the habit of smoking or drinking may be more susceptible to BP.

Benzene ; poisoning ; Case-Control Studies ; Ethanol ; adverse effects ; Genotype ; Glutathione Transferase ; genetics ; Humans ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; Occupational Diseases ; genetics ; Occupational Exposure ; Polymorphism, Single Nucleotide ; Smoking ; adverse effects