The isolation of an antimycin A-resistant human cell line

An antimycin A-resistant derivative of the human cell line, D98, has been obtained by selective mutagenesis with N-methyl-N'-nitro-N-nitrosoguanidine. The derivative, designed MA65, is capable of continuous growth in 15 microM antimycin and the resistant phenotype is stable in the absence of selection. MA65 is not cross-resistant to chloramphenicol or triethyl tin. Crude membrane preparations from MA65 after propagation in medium containing antimycin have normal succinate-cytochrome c oxidoreductase activity and the respiratory activity of whole cells continues in the presence of the drug. The mitochondrially synthesized proteins of D98 and MA65 are similar when compared on sodium dodecyl sulphate (SDS), or isoelectric focusing gels, but there is a reproducible difference in the extent of labelling of one band detected by isoelectric focusing. Genetic analysis is consistent with the existence of a cytoplasmically localized determinant conferring resistance.     

Molecular chaperones in biology and medicine at Obernai

No Abstract Available     

Electron-microscopic study of the rat masseter muscle following injection of lidocaine

The ultrastructure of rat masseter muscle was examined at 15 min, 1 and 6 h, and 1 and 2 days following a single injection of 2% lidocaine. Lesions developed within 15 min. The plasma membrane was disrupted and invaginated. The nuclei were pyknotic and the mitochondria appeared swollen. The myofibrils separated and became disoriented. By 1 and 6 h, these changes were severe. By 1 day, the macrophages appeared in damaged myofibers. The presence of a few presumptive myoblasts signaled the onset of regeneration. By 2 days, presumptive myoblasts formed within the basement membrane. The basal lamina proved most resistant to injury. Regeneration of masseter muscle following the damage produced by lidocaine appeared discontinuous in nature. The singly nucleated presumptive myoblasts seemed to arise within the lesions.