Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term application up to 8 weeks of a 10% urea solution provokes an epidermal thinning expressed in a decreased number of DNA-synthetizing cells. This epidermal reaction cannot be established after topical use of HTH emulsion. Even by daily application during 8 weeks no change was seen. The absence of epidermal thinning after HTH exposure can be explained as an additive effect of urea and the other constituents of the HTH emulsion. This opinion is supported by the results after application of urea together with Tween 60 in that the acanthogenic effect of Tween 60 is decreased by addition of urea. On the other side, the therapeutic efficiency of 10% 5-fluorouracil solution can be increased remarkably by preliminary treatment with HTH emulsion. These findings could reach importance in the topical therapy with regard to the possibility to improve the effectiveness of any drug by addition of, or preliminary treatment with, urea.
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PMID:[Therapeutical action of urea on the skin (author's transl)]. 89 18

To understand the mechanisms of toxicity of hexavalent chromate (K(2)CrO(4), Cr(6+)), the effects of this metal ion on the organization of microtubules (MTs) and microfilaments (MFs), DNA synthesis, cytoskeletal protein synthesis, cytoskeletal protein sulphhydryls (-SH groups), and cellular glutathione (GSH) levels in 3T3 cells were examined. Exposure of cells to Cr(6+) for 16 hr resulted in a dose-dependent inhibition of DNA synthesis with 50% inhibition occurring at 16.6 mum. Treatment of cells with 3.13 mum-Cr(6+) for 16 hr resulted in a slight cell retraction and, in some cells, MT bundling, without much effect on the morphology of dense MFs. At 25 mum, Cr(6+) caused disruption of the cell sheet, depolymerization of MTs, particularly those in the peripheral areas, and redistribution of MFs, which assumed a smearing morphology. Exposure to 100 mum-Cr(6+) induced severe thinning of MTs and loss of MFs. Although doses of 3.13 mum-Cr(6+) or less slightly enhanced the level of cytoskeletal protein synthesis (e.g. 38% increase at 3.13 mum-Cr(6+)), Cr(6+) at 6.25 mum or more produced a dose-dependent inhibition of cytoskeletal protein synthesis (50% inhibition at 11.25 mum). Exposure of cells to Cr(6+) for 16 hr resulted in a dose- and time-dependent increase of cellular GSH level. Furthermore, the elevated cellular GSH induced by Cr(6+) was diminished by treatment with buthionine sulphoximine (BSO), a potent inhibitor of GSH biosynthesis. In addition, depletion of GSH by BSO increased cell sensitivity to Cr(6+) insult and aggravated Cr(6+)-induced cytoskeletal perturbation. However, Cr(6+) treatment of cells did not significantly affect the amount of cytoskeletal protein sulphhydryls. These results suggest that cytoskeletal injury may be an important part of the mechanism for Cr(6+) toxicity. The cytoskeletal damage may result directly from the inhibition of cytoskeletal protein synthesis rather than from the interaction between Cr(6+) and cytoskeletal protein sulphhydryls.
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PMID:Cytoskeletal injury induced by hexavalent chromate. 2073 42