By A. V. S. de & Julie Knight. Reuck
Chapter 1 mobile harm and Alkylation of phone elements (pages 1–29): P. N. Magee
Chapter 2 The Cytotoxic impression of Leucocidin (pages 30–52): A. M. Woodin and A. A. Wieneke
Chapter three Mechanism of motion of definite Exogenous poisonous brokers in Liver Cells (pages 53–73): ok. R. Rees
Chapter four Endogenous Mechanisms of damage in terms of irritation (pages 74–86): W. G. Spector and D. A. Willoughby
Chapter five Interactions among lifeless Cells and residing Tissue (pages 87–105): G. Majno
Chapter 6 mobile harm within the baby Animal (pages 106–122): M. J. R. Dawkins
Chapter 7 Microsomal Peroxidation of Lipids and its attainable position in mobile damage (pages 123–135): P. Hochstein and L. Ernster
Chapter eight mobile accidents attributable to Folic Acid Antagonists and Somec Orticosteroids (pages 136–166): W. Jacobson
Chapter nine Interactions generating harm or fix of mobile Membranes (pages 167–186): A. D. Bangham
Chapter 10 attainable position of Ion Shifts in Liver harm (pages 187–208): J. D. Judah, okay. Ahmed and A. E. M. Mclean
Chapter eleven nice Structural Lesions prompted via Viruses (pages 209–247): W. Bernhard
Chapter 12 Electron Microscopy of Liver and Kidney Cells in nutritional Deficiencies (pages 248–286): W. S. Hartroft
Chapter thirteen stories on cellphone affliction and loss of life: An test at type (pages 287–328): M. Bessis
Chapter 14 The loss of life of Cells in common Multicellular Organisms (pages 329–351): J. D. Biggers
Chapter 15 managed Degeneration in the course of improvement (pages 352–386): E. Zwilling
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Additional info for Ciba Foundation Symposium - Cellular Injury
The loss of mechanical rigidity has been mentioned above. The cell also swells to have about twice the water content of the normal cell, an effect that can be prevented by adding dextraii to the medium. The loss of potassium and gain of sodium and the retention of the amino acids and reducing sugars are not affected (Woodin and Wieneke, unpublished results) but the cell loses more orthophosphate and also some adenosine triphosphate. A further feature is that aldolase appears in the cell supernatant.
188, 420. SCHOENTAL, SCHOENTAL, R. (1961). Nature ( h i d . ) , 192. 670. ,and MAGEE,P. N. (1962). ]. Cutrcer, 16,92. S. ,and SCHLENR, F. (1960). Advmc. , 22, 237. SHAPIRO, SIDGWICR. V. (1942). The Organic Chemistry of Nitrogen, p. 274. London : Oxford University Press. SRINIVASAN, P. , and BORER, E. (1963). Roc. riat. Acad. Sd. ),49, 529. STEKOL, J. , and PERRY, J. (1960). ]. bid. C h i . , 235. PC59. P. (1962). , J CU ~, ~651. DISCUSSION Judah: Since one gets methylation of guanine from S-adenosylmethionine-and one assumes that methionine is not a carcinogen-can you show a greater formation of 7-methylguanine when labelled dimethylnitrosamine is the source of the methyl group than when methionine is the source ?
At I * 4 mM calcium, I 5 mM ATP is optimal and higher concentrations are inhibitory. At all AT” concentrations investigated, calcium concentrations above 2-o mM inhtbit extrusion. Magnesium has an inhibitory action, the extent of which is dependent upon the calcium concentration (Woodin and Wieneke, 1964). The complex interrelationship of the calcium and ATP concentrations permitting extrusion suggests that while both calcium and ATP are necessary for the process to occur, both must be removed for its successful completion.