ArticleMolecular and cellular biochemistry2006
Treatment with dehydroepiandrosterone (DHEA) stimulates oxidative energy metabolism in the liver mitochondria from developing rats.
Article in Molecular and cellular biochemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Steroid hormone regulation of immunometabolism and inflammation.Frontiers in immunology · 2025Review
- Dehydroepiandrosterone Ameliorates Abnormal Mitochondrial Dynamics and Mitophagy of Cumulus Cells in Poor Ovarian Responders.Journal of clinical medicine · 2018Article
- Effect of treatment with cadmium on structure-function relationships in rat liver mitochondria: studies on oxidative energy metabolism and lipid/phospholipids profiles.The Journal of membrane biology · 2009Article
- Stimulation of oxidative energy metabolism in liver mitochondria from old and young rats by treatment with dehydroepiandrosterone (DHEA). A comparative study.Age (Dordrecht, Netherlands) · 2007Article
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2 authors at 1 institution in 1 country.
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Abstract
Effects of treatment with DHEA (0.2 mg or 1.0 mg / kg body weight for 7 days) on oxidative energy metabolism on liver mitochondria from developing and young adult rats were examined. Treatment with DHEA resulted in a progressive dose-dependent increase in the liver weights of the developing animals without change in the body weight. In the young adult rats treatment with 1.0 mg DHEA showed increase only in the body weight. Treatment with DHEA stimulated state 3 and state 4 respiration rates in developing as well as young adult rats in dose-dependent manner with all the substrates used; magnitude of stimulation was age-dependent. In young adults the extent of simulation of state 3 respiration rates declined at higher dose (1.0 mg) of DHEA with glutamate and succinate as substrates. Stimulation of state 3 respiration rates was accompanied by increase in contents of cytochrome aa3, b and c + c1 and stimulation of ATPase and dehydrogenases activities in dose- and age-dependent manner.
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