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Glucocorticoid effects on the embryonic chick heart. II. Alteration of oxidative metabolism
Insights
Cortisol phosphate injection impairs embryonic chick heart mitochondria function, reducing oxygen consumption and ATP production. This suggests a defect in mitochondrial phosphorylation, impacting energy transduction.
Area of Science:
- Biochemistry
- Developmental Biology
- Mitochondrial Physiology
Background:
- Glucocorticoids like cortisol play crucial roles in development.
- Mitochondrial function is vital for cellular energy production and homeostasis.
Purpose of the Study:
- To investigate the effects of cortisol phosphate on embryonic chick heart mitochondrial function.
- To determine the impact of cortisol on oxygen consumption, ATP production, and calcium handling.
Main Methods:
- Cortisol phosphate was injected into embryonic chick eggs.
- Heart mitochondria were isolated 24 and 48 hours post-injection.
- Oxygen consumption, ATP production, and calcium accumulation were measured using various substrates.
Main Results:
- Cortisol injection significantly depressed mitochondrial oxygen consumption and ATP production.
- Impaired phosphorylation was observed with flavin adenine dinucleotide (FADH)-linked substrates (site 2), but not reduced nicotinamide-adenine dinucleotide (NADH)-linked substrates (site 1).
- Cortisol also reduced calcium accumulation by mitochondria.
Conclusions:
- Cortisol phosphate induces mitochondrial dysfunction in embryonic chick hearts.
- A specific defect in site 2 phosphorylation is suggested, distinct from site 1 energy transduction.
- The precise mechanism, whether membrane turnover, calcium overload, or constituent digestion, requires further investigation.
Abstract:
The injection of cortisol phosphate (0.5 mg per egg) onto the chorioallantoic membrane of embryonic chicks at 12 days incubation depresses the rate of oxygen consumption in heart mitochondria isolated from the chicks 24 or 48 hours after the injection as compared to a saline injected control. The oxygen consumption is depressed using either reduced nicotinamide-adenine dinucleotide (NADH)-linked or flavin adenine dinucleotide (FADH)-linked substrates. The progressive inhibition of oxidation and adenosine triphosphate (ATP) production rate is related to the time after cortisol is injected. The treated mitochondria appear to function differently when NADH-linked and FADH-linked respiratory substrates are compared. Using NADH-linked substrates (site 1), adenosine diphosphate (ADP) was phosphorylated by mitochondria, even though the rate of phosphorylation was decreased; however, when FADH-linked substrates were used, incomplete phosphorylation was observed. The rate and the extent of calcium accumulation by embryonic chick heart mitochondria were also depressed by cortisol. These data suggest a defect in phosphorylation at site 2 following cortisol treatment but not at the site 1 linked energy transducing step. Whether these impairments of mitochondrial function result from catabolic turnover of the mitochondrial membrane components, excessive calcium accumulation by the mitochondria, or from the digestion of mitochondrial constituents, has not been delineated.
