Abstract
Rat parotid gland slices showed a very slow rate of glucose utilization and lactic acid production, both in the presence and in the absence of oxygen. Epinephrine, which caused rapid enzyme secretion by the slices did not affect the low rate of glycolysis.A rough calculation indicates that in the parotid gland ATP is produced by oxidative phosphorylation 50 times faster than by glycolysis. The mitochondria, when isolated and tested in presence of EDTA or EGTA showed respiratory activity and respiratory control comparable to those of liver mitochondria. Adenosine 3′ : 5′‐cyclic phosphate, which is an intermediate in induction of enzyme secretion, showed no clear‐cut effect on the functions of the parotid mitochondria. Isolation of the mitochondria in the absence of the above chelators yielded a preparation which was almost depleted of NAD, respired feebly on NAD linked substrates and showed no respiratory control. Addition of NAD+ restored respiration. The damage caused to these mitochondria during isolation was attributed to the high calcium concentrations found in the gland. Addition of small amounts of free calcium to functional parotid mitochondria indeed caused the loss of NAD and the decline of respiration. Tested in parallel experiments, liver mitochondria were much more resistant to added calcium. Their initial calcium content was one tenth that of the parotid mitochondria. The control of calcium distribution in the parotid gland and the possible functions of calcium are discussed.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.