Intact Ehrlich ascites tumour cells exhibit a residual respiration which is insensitive to site-specific inhibitors of mitochrondrial electron transport. Treatment of the tumour-bearing mice with phenobarbital does not influence the rate of this inhibitor-resistant respiration. 2. Among the respiratory pigments analysed spectrophotometrically in the microsomal fraction prepared from ascites cells, only small amounts of flavoproteins (NADH-cytochrome b5 reductase and NADPH-cytochrome c reductase) were detectable. 3. Ascites-cell nuclei respire with NADH or NADPH, but not with succinate, as substrates and the respiration is unaffected by inhibitors of mitochondrial electron and energy transfer. These nuclei contain cytochrome b5, whereas cytochrome P-450 or mitochondrial-like cytochromes are lacking. 4. It is concluded that the NAD(P)H-dependent electron transport in nuclei is responsible for the inhibitor-insensitive O2 uptake of intact cells. Conversely, mixed function oxidation reactions of the endoplasmic reticulum have no role in this connection. Moreover, it is assumed that nuclear respiration is involved in the control of the cellular redox potential. 5. The relevance of the data obtained with respect to some assumptions concerning the biogenesis of the endoplasmic reticulum is discussed.
