KY 405364236. USA Cigarette smoking constitutes a major source of cadmium exposure via inhalation in man. To determine how smoke exposure affects the organ distribution and accumulation of cadmium, male C57B1 mice and Sprague-Dawley rats were exposed daily for 52-60 consecutive weeks to mainstream s
Induction by cigarette smoke of aryl hydrocarbon hydroxylase activity in the rat kidney and lung1
β Scribed by Jacques Van Cantfort; Jacques Gielen
- Publisher
- John Wiley and Sons
- Year
- 1977
- Tongue
- French
- Weight
- 699 KB
- Volume
- 19
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
β¦ Synopsis
Abstract
In both the rat kidney and lung, inhalation of cigarette smoke diluted with air (1/15) for a limited period of time (15 min) specifically induces aryl hydrocarbon hydroxylase (AHH)<2> in less than 4 h. Up to four successive inhalations administered at 2βh intervals additively induce both lung and kidney hydroxylase activities. The maximal effect corresponds to about 10 times the control value. Compared to the kidney enzyme, the lung AHH activity is about three or four times more sensitive to small concentrations of cigarette smoke. The biological halfβlife of the lung AHH activity is longer than 24 h, while it is only 3β4 h in the kidney. In both tissues, the induced enzyme presents the same in vitro thermolability and sensitivity to various inhibitors. For the establishment of the AHH induction, protein synthesis is continuously required, while RNA synthesis is only necessary during the first 2 h following the smoke treatment.
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