Mitochondrial proliferation within the nephron. I. Comparison of mitochondrial hyperplasia of tubular regeneration with compensatory hypertrophy.
MITOCHONDRIAL PROLIFERATION IN THE RENAL PROXIMAL TUBULAR EPITHELIUM IN RESPONSE TO TISSUE LOSS HAS BEEN QUANTITATED BY TWO DIVERSE MODELS: acute tubular necrosis induced by mercuric chloride and unilateral nephrectomy. The increased work demand on the remaining tubular mass in both models has probably stimulated both cell hyperplasia and hypertrophy. In both instances, cell hyperplasia preceeds hypertrophy. During the cellular hypertrophy, mitochondria first proliferate in number and then increase in size; presumably to satisfy the greater need for energy metabolism necessary during increased active transtubular solute transport.
D000818:Animals; D001345:Autoradiography; D002467:Cell Nucleus / Q000032:analysis; D004272:DNA, Mitochondrial / Q000096:biosynthesis; D004847:Epithelial Cells; D006965:Hyperplasia / Q000473:pathology; D006984:Hypertrophy / Q000473:pathology; D007668:Kidney / Q000473:pathology*; D007687:Kidney Tubules, Proximal / Q000473:pathology; D008297:Male; D008628:Mercury; D008854:Microscopy, Electron; D008928:Mitochondria / Q000378:metabolism; D008938:Mitosis; D009336:Necrosis / Q000139:chemically induced; D009392:Nephrectomy; D009399:Nephrons / Q000473:pathology; D051381:Rats; D013936:Thymidine / Q000378:metabolism; D014316:Tritium
D004272:DNA, Mitochondrial; D014316:Tritium; D008628:Mercury; D013936:Thymidine