Enhancement of XXXX skin @entity105 by inhibiting cell proliferation with @entity1862 or skin extracts.

@entity7045 @entity19 @entity1862 @entity1489 @entity5 @entity1324 @entity7044 @entity105
To study the relationship between epidermal DNA synthesis and @entity105 , groups of hairless @entity19 were given a single skin application of 2 mg @entity7044 ( @entity7045 ) in @entity1324 . One group received no pretreatment, another group was injected i.p. with 5 mg @entity1862 (HU) 30 min before @entity7045 , and a further group with 0.5 mg Colcemid 3 h before @entity7045 . Other groups were injected i.p. 14 and 4 h before @entity7045 with either saline, 5 mg crude aqueous skin extract, 2 mg dialysed skin extracts of two types, or 2 mg dialysed extracts of liver or heart muscle, respectively. All substances were dissolved in 0.5 ml distilled water. Cell kinetic studies showed that the three skin extracts inhibited epidermal DNA synthesis and mitosis. HU inhibited DNA synthesis and increased the mitotic rate. The other pretreatments had no effect on epidermal DNA synthesis. There was a significant enhancement of the production of @entity1489 in the groups pretreated with epidermal extracts or HU. @entity7045 is a short-acting carcinogen with a half-life in the cell of 30 min. Hence, the results show that when DNA synthesis is inhibited at the time of @entity7045 application, more @entity5 are produced in the skin. A possible explanation of the enhancement is that a compensatory wave of proliferation a short time after carcinogen binding may fix a DNA injury before repair can take place.
