Benzoyl peroxide, a widely used free radical-generating compound, promoted both papillomas and carcinomas when it was topically applied to mice after 7,12-dimethylbenz[a]anthracene initiation. Benzoyl peroxide was inactive on the skin as a complete carcinogen or as a tumor initiator. A single topical application of benzoyl peroxide produced a marked epidermal hyperplasia and induced a large number of dark basal keratinocytes, effects similar to those produced by the potent tumor promoter 12-O-tetradecanoyl phorbol-13-acetate. Benzoyl peroxide, like other known tumor promoters, also inhibited metabolic cooperation (intercellular communication) in Chinese hamster cells. In view of these results caution should be recommended in the use of this and other free radical-generating compounds.
Downloaded from 84 SLACA ET AL.There is a good correlation between the tumor-initiating activities of PAH and their abilities to bind covalently to DNA. In addition, various inhibitors of PAH tumor initiation show a strong correlation with their abilities to inhibit the binding of the PAH to DNA and their anti-tumor initiating activities. There is also a good correlation between the promoting abilities of phorbol esters to promote tumors and their abilities to induce ornithine decarboxylase (ODC), cell proliferation and dark basal keratinocytes. When other nonpromoting hyperplastic agents are used, only dark cell induction correlates with promotion. Certain polyamines and prostaglandins can enhance phorbol ester tumor promotion. Anti-inflammatory steroids, retinoids, and protease inhibitors are potent inhibitors of tumor promotion. They inhibit tumor promotion by inhibiting either the 7 2-0-tetradecanoylphorbol-13 -acetate (TPA) induced cell proliferation, ODC and/or dark basal keratinocytes. Certain weak promoters such as mezerein which mimics TPA in many biochemical and morphological effects are potent second step promoters in a two-stage promotion regimen.6 . Co-initiating and Co-promoting Agents 7. Anti-carcinogenesis 8.
Extracts of soots obtained from various sources were applied to the skin of mice in an effort to identify carcinogens in these mixtures and to link these materials to the etiology of human cancer. Samples of coal chimney soot, coke oven materials, industrial carbon black, oil shale soot, and gasoline vehicle exhaust materials have been examined by this method. The studies reported here have been constructed to compare the carcinogenic and tumorigenic potency of extracts from various particulate emissions: coke ovens, diesel and gasoline vehicles and a roofing tar pot. Automobile emission samples were obtained by collecting the diluted and cooled exhaust on Teflon-coated glass fiber filters. Coke oven and roofing tar samples were particulate emission samples collected by impaction and filtration. The organic components associated with each of the particles were extracted with dichloromethane and dermally applied to SENCAR mice. All agents were applied as tumor initiators by using a five-dose protocol. Selected extracts were also applied as complete carcinogens and as tumor promotors. Statistical analyses of the resulting tumor data were performed by using nonlinear Poisson and probit models. The results from these experiments provide a suitable data base for comparative potency estimation of complex mixtures.
Abstract. Excised apical portions of green wheat leaf sections were treated with amino. triazole to prevent formation of new ohloroplasts. Illumination retarded the decline in chlorophyll content per leaf section, the disintegration of chloroplast ultrastruoture, and the loss of capacity for photosynthetic carbon fixation. We interpret these 3 effects of illumination as facets of a single light effect in retarding chloroplast senescence. This light effect in retarding chloroplast senescence has features differing from characteristics of photosynthetic carbon fixation. For example, A) application of the photosynthetic inhibitor 3-(3,4-dichlorophenyl)-1, 1-dimethylurea did not decrease, and may have even slightly increased, the effectiveness of light; B) although the action spectrum contains peaks in the blue and red regions, it differs from the action spectrum for photosynthetic CO2 sssimilation in wheat; C) in nonphotosynthesizing tissue, application of sugars did not retard chloroplast senescence; D) light saturation was achieved by only a few hundred microwatts/cm2. Considered together with the well-known light requirement for chloroplast formation, our results indicate that light has a dual, photomorphogenetic control in maintaining the green status of the plant by also exerting a second effect: retarding of senescence of chloroplasts already present.It is common knowledge that leaves are greelner in the light than in the dark and that in most higher plants light is necessary for the formation of the photosynthetic apparatus. The work described in this paper was begun to see to what extent, if any, light could control the photosynthetic capacity of leaves by also controlling functional and ultrastructural aspects of senescence of chloroplasts already formed.In general, when iboth chloroplast formation and chloroplast disintegration can occur, it may be difficult'to unravel the 2 processes, formation and disintegration, in the maintenance of numbers of intact, mature chloroplasts. A study of chloroplast disintegration in light and in darkness is greatly simplified by use of aminotriazole (AT) 2, a chemical that prevents normal chloroplast formation even in the light. AT has no other pronounced effects on overall metabolism in leaves of young wheat seedlings (1). When chloroplast formation is absent in wheat leaf tissue in darkness, chloroplast disintegration is indicated by the decline in chlorophyll content (6,16). We now report and describe the effects of light in retarding chloroplast senescence in leaf chlorenchyma of young wheat seedlings.
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