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SUMMARY Apoptosis is an important tool for shaping developing organs and for maintaining cellular homeostasis. In the colonial urochordate Botryllus schlosseri, apoptosis is also the hallmark end point in blastogenesis, a cyclical and weekly developmental phenomenon. Then the entire old generation of zooids are eliminated (resorbed) by a process that lasts 24–36 h. Administration of the antioxidant butylated hydroxytoluene (BHT) resulted in resorption being arrested by 1–8 days on average. At high doses(2.5–15.0 mg BHT l-1) resorption was completed only after removal of BHT. Colonies that were not removed in time, died. In treated colonies, although DNA fragmentation was high, tissues and organs that would normally have died, survived, and the general oxidative levels of lipids were reduced. Blood vessels were widened, containing aggregates of blood cells with a significantly increased proportion of empty macrophage-like cells without inclusion. In colonies rescued from BHT treatment, resorption of zooids started immediately and was completed within a few days. We propose three possible mechanisms as to how BHT may affect macrophage activity: (1) by interrupting signals that further promote apoptosis; (2) through the respiratory burst initiated following a phagocytic stimulus; and (3) by reducing lipid oxidation and changing cell surface markers of target cells. Our results point, for the first time, to the role of phagocytic cells in the coordination of death and clearance signals in blastogenesis.

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Aging of skeletal muscle in the hindleg of the mouse is accompanied by a progressive increase in the amount of the interstitial tissue and especially that of lipid cells and fibroblasts. Quantitative analysis indicates that there was a nonsignificant increase in the total number of muscle fibers per unit area, perhaps due to a splitting process. The proportion of high oxidative fibers was decreased to a nonsignificant degree, and the remaining high oxidative fibers underwent a significant compensatory hypertrophy. Concomitantly, the number of low oxidative fibers increased significantly. This study revealed that endurance training in young animals induced morphometric changes very similar to those noticed in intact aging animals (i.e., splitting phenomenon, hypertrophy of high oxidative fibers, and an increased proportion of low oxidative fibers). It also became apparent that the skeletal muscle of old animals lacks the capacity to respond to enforced training, except for a further increase in the proportion of low oxidative fibers. It appears that aging muscle is unable to adapt to changing environmental circumstances.