Mitochondrial DNA mutations in human colonic crypt stem cells
J. Clin. Invest. Robert W. Taylor, et al. 112:1351 doi:10.1172/JCI19435 [Go to this article.]

Figure 1
Respiratory chain deficiency in normal human colonic mucosa. (a) H&E preparations showing normal mucosal structure. Scale bar: 100 μm. (b) Higher magnification of a, showing normal crypt structure. Scale bar: 50 μm. (c) Normal cytochrome c oxidase activity (brown) in colonic crypts following dual cytochrome c oxidase and succinate dehydrogenase histochemistry. Scale bar: 100 μm. (d) Absence of histochemically detectable cytochrome c oxidase activity in colonic crypts (blue). Note delineation of crypt territories at the luminal surface. Scale bar: 100 μm. (e) Single cytochrome c oxidase–deficient colonic crypt. Scale bar: 100 μm. (f) Higher magnification of e, showing crypt base. Scale bar: 20 μm. (g) Presence of multiple, adjacent cytochrome c oxidase–deficient crypts. Scale bar: 100 μm. (h) Transverse section showing a similar cluster of cytochrome c oxidase–deficient crypts. Scale bar: 100 μm. The specificity of the dual cytochrome c oxidase and succinate dehydrogenase histochemical assay was established. (i) Colonic mucosa incubated in standard cytochrome c oxidase medium. (j) Colonic mucosa incubated as i, but in the presence of 2.5 mM sodium azide, a specific inhibitor of cytochrome c oxidase. (k) Colonic mucosa incubated in standard succinate dehydrogenase medium. (l) Colonic mucosa incubated as k, but in the presence of 50 mM sodium malonate, a competitive inhibitor of succinate dehydrogenase. Scale bars: 100 μm (i–k).