Lipofuscin formation in the myocardium of juvenile golden hamsters: an ultrastructural study including staining for acid phosphatase.

Atrial and ventricular myocardium from young golden hamsters, 3-6 months of age, was examined under the transmission electron microscope, representative samples from each animal having been stained histochemically for acid phosphatase (AP) by a lead precipitation technique. Our observations indicated that AP positive primary lysosomes are produced at the sites of Golgi-endoplasmic reticulum-lysosome (GERL) complexes and the main pathway for lipofuscin production is by fusion of primary lysosomes with mitochondria in both atrial and ventricular myocytes. The mitochondria are then progressively degraded, their matrix becomes denser and there is an accompanying increase of AP activity. After reaching a peak level, AP activity declines until an AP negative terminal pigment body with a smooth outline is produced. Another pathway, but much less frequent at this age leads to the formation of larger bodies, irregular in outline and containing small globules. Their genesis entails the participation of autophagic vacuoles which engulf lipid droplets, mitochondria or amorphous debris. Like the main variety of lipofuscin body, they contain AP while digestion progresses but eventually become AP negative. A few lipofuscin granules are eliminated by being pinched off within fine cell protrusions and are subsequently engulfed by scavenger cells.