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Salinity adaptation in fish: effect of thyroxine on mitochondrial status
Archives of Biochemistry and Biophysics
|September 1, 1984
Summary
Transferring freshwater fish to seawater significantly alters gill mitochondria function, impacting energy production and ion transport. Thyroxine administration effectively reverses these stress-induced changes, suggesting a role in mitochondrial restoration.
Area of Science:
- Physiology
- Biochemistry
- Environmental Science
Background:
- Freshwater fish (Sarotherodon mossambicus) face physiological challenges when transferred to saline environments.
- Gill mitochondria are crucial for energy metabolism and ion regulation, and are likely affected by osmotic stress.
Purpose of the Study:
- To investigate the functional changes in gill mitochondria of Sarotherodon mossambicus upon transfer to 50% seawater.
- To determine the effect of thyroxine administration on these stress-induced mitochondrial alterations.
Main Methods:
- Monitoring key mitochondrial functions including ADP/O ratio, respiratory control index (RCI), ATP-Mg2+ induced contraction, and energy-dependent 45Ca uptake.
- Assessing amino acid incorporation capacity, adenine nucleotide content, and endogenous Ca2+ levels.
- Administering thyroxine to stressed fish and evaluating the reversal of mitochondrial dysfunction.
Main Results:
- Transfer to 50% seawater caused loss of ADP/O and RCI, impaired ATP-Mg2+ induced contraction, and reduced energy-dependent 45Ca uptake.
- Increased amino acid incorporation, adenine nucleotide content, and endogenous Ca2+ were observed in mitochondria from fish in 50% seawater.
- Thyroxine administration effectively reversed these functional changes in gill mitochondria, with sustained effects.
Conclusions:
- Osmotic stress significantly disrupts gill mitochondrial function in Sarotherodon mossambicus.
- Thyroxine plays a vital role in restoring mitochondrial function under osmotic stress, potentially by promoting mitochondriogenesis.