The effect of recombinant human growth hormone and insulin-like growth factor-1 on the mitochondrial function and viability of peripheral blood mononuclear cells in vitro

James Keane*, Lotti Tajouri, Bon Gray

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

4 Citations (Scopus)

Abstract

This study investigated whether the putative physiological benefits induced by growth hormone (GH) and insulin-like growth factor-1 (IGF-1) are countered at supra-physiological concentrations because of an augmentation in the production of mitochondrial-derived free radicals with a subsequent increase in oxidative damage, compromising mitochondrial function. To test this hypothesis, peripheral blood mononuclear cells were incubated for 4 h with either recombinant human GH (rhGH) (range = 0.25–100 μg/L) or recombinant IGF-1 (rIGF-1) (range = 100–600 μg/L) and along with control samples were subsequently analyzed by flow cytometry for the determination of cellular viability, mitochondrial membrane potential (Δψm), mitochondrial superoxide (O2 ) generation, and mitochondrial permeability transition pore (mtPTP) activity. Results showed levels of mitochondrial O2 generation to be significantly reduced compared with control samples (lymphocytes: 21.5 ± 1.6 AU; monocytes: 230.2 ± 9.8 AU) following rhGH treatment at both concentrations of 5 μg/L (13.5 ± 1.3 AU, P ≤ 0.05) and 10 μg/L (12.3 ± 1.5 AU, P ≤ 0.05) in lymphocytes and at 10 μg/L (153.4 ± 11.4 AU, P ≤ 0.05) in monocytes. However, no significant effect was found at either higher rhGH concentrations or following treatment with any concentration of rIGF-1. In addition, neither of the 2 hormones had any significant effect on Δψm, mtPTP activity, or on cellular viability. In conclusion, physiological concentrations of rhGH elicited a protective cellular effect through the reduction of oxidative free radicals within mitochondria. This antioxidant effect was diminished at supra-physiological concentrations but not to a level that would elicit disruption of mitochondrial function.

Original languageEnglish
Pages (from-to)105-115
Number of pages11
JournalApplied Physiology, Nutrition and Metabolism
Volume40
Issue number2
DOIs
Publication statusPublished - 16 Oct 2014

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