[Gender-dependent Expression of ERß in AEC â ¡ of Fetal Mice Exposed to Arsenic and Estrogen Receptor Antagonist].

OBJECTIVE: To determine the effects of arsenic and estrogen receptor antagonist (ICI182, 780) on the expression of estrogen receptor beta (ERß) in alveolar Ⅱ epithelial cells (AECⅡ) of female and male mice. METHODS: Nineteen or twenty day fetus mice were obtained through caesarean section of ICR mice. Purified AECⅡ cells were separated from the female and male fetus,respectively,and confirmed using immunofluorescence staining. The cells were exposed to sodium arsenite (NaAsO2) at a low,medium,or high dosage determined by MTT and cultured for 24 h. The NaAsO2 (5 µmol/L) exposed cells were compared with those treated (for 24 h) with dimethyl sulfoxide (DMSO) or ICI182, 780 (1×10-4 mol/L). Apoptosis rates of the cells were measured by flow cytometry. Real-time fluorescence quantitative PCR method and Western blot technique were used to detect the expression ofERßmRNA and protein in AECⅡ. RESULTS: Purity of AECⅡ cells reached (87.0±2.5)%. NaAsO2 exposure was set at a concentration of 0.5 (low),1.25 (medium),and 5 (high) µmol/L. The cells exposed to medium and high dosage of NaAsO2 had higher apoptosis rates than the blank controls (P<0.05),without sex differences. Female cells exposed to medium and high dosage of NaAsO2 had higher levels of expressions ofERßmRNA and protein than the blank controls (P<0.05) and male cells exposed to the same dosage of NaAsO2 (P<0.05). No significant differences were found in the expressions ofERßmRNA and protein between the exposed male cells and the blank controls. ICI182, 780 lowered the expression levels ofERßmRNA and protein in the female exposed cells (P<0.01). CONCLUSION: Arsenic exposure increases expressions of AECⅡ's ERß,more so in female cells than in male cells. This can be blocked by estrogen receptor antagonists.

[The Relationship of Polymorphisms in Interleukin 17A Gene, Interleukin 17F Gene and the Pulmonary Inflammation Risk in Dust Exposed Workers in a Chinese Population].

OBJECTIVES: To investigate the polymorphisms in interleukin 17A IL-17A) and interleukin 17F (IL-17F) and their relationship with pulmonary inflammation risk of dust exposed workers. METHODS: A case-control study among 193 subjects, including 67 subjects in case group and 126 in control group was conducted. PCR-RFLP was applied to genotype IL-17A (G-197A) and IL-17F (7488T/C). Logistic regression analysis was used to determine the effects of IL-17A (G-197A) and IL-17F (7488T/C) on the lung inflammation risk in dust exposed workers. RESULTS: The genotypes analysis showed that the proportions of IL-17A (G-197A) A/A, A/G and G/G were 42 (21.76%), 95 (49.22%), 56 (29.02%) in 193 cases, respectively, and the IL-17F (7488T/C) T/T, T/C and C/C genotypes were 128 (66.32%), 54 (28.98%), 11 (5.70%), respectively. The frequency distribution of each genotype was consistent with the Hardy-Weinberg equilibrium fixed law. The ratio of IL-17A (G-197A) A/A in the case group was lower than that of control group ( P<0.05), while the G/G and A/G genotypes were higher than that of control group ( P<0.05). Furthermore, the genotypes of IL-17A (G-197A) A/G (OR=5.03, P<0.01) and G/G(OR=3.35, P<0.05) were associated with an increased risk of lung inflammation in workers exposed to dust. The frequency distribution difference of IL-17F (7488T/C) T/T, T/C and C/C genotypes in the cases and control group was unobvious ( P>0.05). CONCLUSIONS: Under the same dust concentration, the dust exposed workers carrying IL-17A (G-197A) A/G, G/G genotypes are more susceptible to pulmonary inflammation in the southwest of China.