[Ultrastructural studies of the effect of x-rays and quinacrine (Atebrin) or chloroquine (Resochin)--alone or in combination--on Harding-Passey melanoma cells in monolayer culture].
{"title":"[Ultrastructural studies of the effect of x-rays and quinacrine (Atebrin) or chloroquine (Resochin)--alone or in combination--on Harding-Passey melanoma cells in monolayer culture].","authors":"R Pfab, D O Schachtschabel, H F Kern","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Monolayer cells of a Harding-Passey melanoma (HPM 73 cells) which were irradiated during the phase of exponential growth with an X-ray dose of 4 Gy of 8 Gy did not show any ultrastructural changes four days after 4 Gy, whereas cells irradiated with 8 Gy showed slight damages such as swollen mitochondria and vacuoles. As shown by the electron microscope, a sole addition of a sublethal quantity (6 X 10(-6) M) of quinacrine (Atebrin) or chloroquine (Resochin) did not lead to significant cell modifications. Those melanoma cells with were pre-irradiated with 8 Gy and then incubated during four days with 6 X 10(-6) M of quinacrine (Atebrin) or 6 X 10(-6) M of chloroquine (Resochin) showed severe damages. There was an increased rate of vacuoles and segregational structures in cytoplasm. The mitochondria were increased and swollen and the cellular surfaces had less microvilli. However, microtubules and microfilaments seemed more distinct. The melanin concentration increased under this treatment. The cell nuclei were increased in volume and seemed to be rather void of chromatin. These reactions of cells on quinacrine (Atebrin) and chloroquine (Resochin) are explained by the known inhibition effect exerted by these substances on DNA synthesis, especially as far as the processes of DNA reparation are concerned. The changes of the microtubule-microfilament system could be due to a correlation with the increase of digestive intracellular processes connected with the catabolism of radiation-damaged structures.</p>","PeriodicalId":21981,"journal":{"name":"Strahlentherapie","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1985-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Strahlentherapie","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
Monolayer cells of a Harding-Passey melanoma (HPM 73 cells) which were irradiated during the phase of exponential growth with an X-ray dose of 4 Gy of 8 Gy did not show any ultrastructural changes four days after 4 Gy, whereas cells irradiated with 8 Gy showed slight damages such as swollen mitochondria and vacuoles. As shown by the electron microscope, a sole addition of a sublethal quantity (6 X 10(-6) M) of quinacrine (Atebrin) or chloroquine (Resochin) did not lead to significant cell modifications. Those melanoma cells with were pre-irradiated with 8 Gy and then incubated during four days with 6 X 10(-6) M of quinacrine (Atebrin) or 6 X 10(-6) M of chloroquine (Resochin) showed severe damages. There was an increased rate of vacuoles and segregational structures in cytoplasm. The mitochondria were increased and swollen and the cellular surfaces had less microvilli. However, microtubules and microfilaments seemed more distinct. The melanin concentration increased under this treatment. The cell nuclei were increased in volume and seemed to be rather void of chromatin. These reactions of cells on quinacrine (Atebrin) and chloroquine (Resochin) are explained by the known inhibition effect exerted by these substances on DNA synthesis, especially as far as the processes of DNA reparation are concerned. The changes of the microtubule-microfilament system could be due to a correlation with the increase of digestive intracellular processes connected with the catabolism of radiation-damaged structures.