کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2597344 | 1132577 | 2007 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Trichloroethylene induce nitric oxide production and nitric oxide synthase mRNA expression in cultured normal human epidermal keratinocytes
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Trichloroethylene induce nitric oxide production and nitric oxide synthase mRNA expression in cultured normal human epidermal keratinocytes Trichloroethylene induce nitric oxide production and nitric oxide synthase mRNA expression in cultured normal human epidermal keratinocytes](/preview/png/2597344.png)
چکیده انگلیسی
Trichloroethylene (TCE), a major chemical hazard during occupational exposure, can cause obvious skin lesions, including irritant reactions and dermatitis. Nitric oxide (NO) synthesized by nitric oxide synthase (NOS) is involved in a broad array of pathogenesis of skin inflammatory and immune responses. To understand the mechanisms of TCE-induced dermatoxicity, we investigated the effects of TCE on NO production and NOS mRNA expression in cultured normal human epidermal keratinocytes (NHEK). Cells were treated with TCE (0Â mM, 0.125Â mM, 0.25Â mM, 0.5Â mM, 1.0Â mM, 2.0Â mM) for 4Â h, and then incubated for 12Â h, 24Â h, 48Â h and 72Â h. At each given time point, NO production were evaluated indirectly by measuring nitrite plus nitrate concentration in the culture medium using Griess reaction, as well as cell viability determined by MTT test, iNOS and cNOS activities assayed with a NOS activity detecting kit. The expression of iNOS and cNOS mRNA was detected using RT-PCR. TCE decreases cell viability and enhance NO production from NHEK in concentration- and time-dependent manner. Aminoguanidine (AG), an inhibitor of NOS, can prevent NO production and cell viability decrease in NHEK by TCE induced. Change to NO production was accompanied by increased activities of both types of NOS, but the iNOS activity accounted mainly for the TCE-induced NO production. RT-PCR detection showed that NHEK expressed both iNOS and cNOS mRNA by TCE exposure. Whereas a concentration- and time-dependent up-regulation of the mRNA expression was observed for iNOS and cNOS following TCE exposure, changes to iNOS were more marked. These results suggest that TCE caused increase in NO production, attributed to activation of iNOS as well as cNOS, and expression of iNOS and cNOS mRNA. These cellular changes may contribute to the pathological and physiological features of TCE-induced erythema and skin inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology - Volume 239, Issue 3, 8 October 2007, Pages 186-194
Journal: Toxicology - Volume 239, Issue 3, 8 October 2007, Pages 186-194
نویسندگان
Tong Shen, Qi-Xing Zhu, Sen Yang, Rui Ding, Tai Ma, Liang-Ping Ye, Li-Jie Wang, Zhao-Zhao Liang, Xue-Jun Zhang,