Matches in Nanopublications for { ?s ?p "others clearly are not [19, 43]. In fact, the ROS-induced modulation of gene expression associated with DNA repair can occur in the absence of DNA damage [44]. Some of the effects of UV radiation exposure on various pathways are probably stimulated by DNA damage; however, UVA radiation (320-380 nm), which produces little DNA damage, is effective at inducing expression of collagenase [45], heme oxygenase [46,47], ICAM-1 [48], IL-10 [49], cjun, c-fos, and activation of the JNK MAP kinase pathway [50] and at stimulating increases in ferritin protein [51]. Furthermore, exposure of cells to singlet oxygen generation without light exposure stimulates collagenase production [52]. Redox changes that alter gene expression are not limited to increases in oxidation. Antioxidant treatments can also stimulate increases in the expression of certain genes [53-57]. Although it is possible that autoxidation of antioxidant compounds produces enough ROS to stimulate changes in gene expression through oxidizing rather than reducing mechanisms, this seems improbable. Keogh et al. [55] examined several parameters of oxidation in fibroblasts stimulated to increase c-fos abundance with different antioxidant compounds and found no evidence of increased oxidation; albeit, the antioxidant effects observed were small and were manifested primarily as an increase in GSH concentration. It is also possible that secondary effects of chemical treatments rather than their oxidant/antioxidant properties are responsible for the effects on signal transduction and gene expression. This too seems improbable, because oxidants have been used to block the effects of antioxidant compounds [25,33,58,59] and vice versa [11,26,36,60-77] in a number of independent studies. Choi and Moore [78] examined a series of structural isomers of butylated hydroxytoluene and observed that only those compounds with relatively high antioxidant potential are capable of inducing c-fos." ?g. }
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- _3 value "others clearly are not [19, 43]. In fact, the ROS-induced modulation of gene expression associated with DNA repair can occur in the absence of DNA damage [44]. Some of the effects of UV radiation exposure on various pathways are probably stimulated by DNA damage; however, UVA radiation (320-380 nm), which produces little DNA damage, is effective at inducing expression of collagenase [45], heme oxygenase [46,47], ICAM-1 [48], IL-10 [49], cjun, c-fos, and activation of the JNK MAP kinase pathway [50] and at stimulating increases in ferritin protein [51]. Furthermore, exposure of cells to singlet oxygen generation without light exposure stimulates collagenase production [52]. Redox changes that alter gene expression are not limited to increases in oxidation. Antioxidant treatments can also stimulate increases in the expression of certain genes [53-57]. Although it is possible that autoxidation of antioxidant compounds produces enough ROS to stimulate changes in gene expression through oxidizing rather than reducing mechanisms, this seems improbable. Keogh et al. [55] examined several parameters of oxidation in fibroblasts stimulated to increase c-fos abundance with different antioxidant compounds and found no evidence of increased oxidation; albeit, the antioxidant effects observed were small and were manifested primarily as an increase in GSH concentration. It is also possible that secondary effects of chemical treatments rather than their oxidant/antioxidant properties are responsible for the effects on signal transduction and gene expression. This too seems improbable, because oxidants have been used to block the effects of antioxidant compounds [25,33,58,59] and vice versa [11,26,36,60-77] in a number of independent studies. Choi and Moore [78] examined a series of structural isomers of butylated hydroxytoluene and observed that only those compounds with relatively high antioxidant potential are capable of inducing c-fos." provenance.
- _4 value "others clearly are not [19, 43]. In fact, the ROS-induced modulation of gene expression associated with DNA repair can occur in the absence of DNA damage [44]. Some of the effects of UV radiation exposure on various pathways are probably stimulated by DNA damage; however, UVA radiation (320-380 nm), which produces little DNA damage, is effective at inducing expression of collagenase [45], heme oxygenase [46,47], ICAM-1 [48], IL-10 [49], cjun, c-fos, and activation of the JNK MAP kinase pathway [50] and at stimulating increases in ferritin protein [51]. Furthermore, exposure of cells to singlet oxygen generation without light exposure stimulates collagenase production [52]. Redox changes that alter gene expression are not limited to increases in oxidation. Antioxidant treatments can also stimulate increases in the expression of certain genes [53-57]. Although it is possible that autoxidation of antioxidant compounds produces enough ROS to stimulate changes in gene expression through oxidizing rather than reducing mechanisms, this seems improbable. Keogh et al. [55] examined several parameters of oxidation in fibroblasts stimulated to increase c-fos abundance with different antioxidant compounds and found no evidence of increased oxidation; albeit, the antioxidant effects observed were small and were manifested primarily as an increase in GSH concentration. It is also possible that secondary effects of chemical treatments rather than their oxidant/antioxidant properties are responsible for the effects on signal transduction and gene expression. This too seems improbable, because oxidants have been used to block the effects of antioxidant compounds [25,33,58,59] and vice versa [11,26,36,60-77] in a number of independent studies. Choi and Moore [78] examined a series of structural isomers of butylated hydroxytoluene and observed that only those compounds with relatively high antioxidant potential are capable of inducing c-fos." provenance.