Administration of Enalapril Started Late in Life Attenuates Hypertrophy and Oxidative Stress Burden, Increases Mitochondrial Mass and Modulates Mitochondrial Quality Control Signaling in the Rat Heart

Anna Picca; Giuseppe Sirago; Vito Pesce; Angela Maria Serena Lezza; Riccardo Calvani; Maurizio Bossola; Emanuele Rocco Villani; Francesco Landi; Christiaan Leeuwenburgh; Christy Carter; Roberto Bernabei; Emanuele Marzetti

doi:10.20944/preprints201809.0234.v1

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preprints.org > biology and life sciences > biochemistry and molecular biology > doi: 10.20944/preprints201809.0234.v1

Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Administration of Enalapril Started Late in Life Attenuates Hypertrophy and Oxidative Stress Burden, Increases Mitochondrial Mass and Modulates Mitochondrial Quality Control Signaling in the Rat Heart

Anna Picca

Giuseppe Sirago

Vito Pesce

Angela Maria Serena Lezza

Riccardo Calvani

^* ,

Maurizio Bossola

Emanuele Rocco Villani

Francesco Landi

Christiaan Leeuwenburgh

Christy Carter

Roberto Bernabei

Emanuele Marzetti

Version 1 : Received: 11 September 2018 / Approved: 13 September 2018 / Online: 13 September 2018 (11:36:07 CEST)

A peer-reviewed article of this Preprint also exists.

Picca, A.; Sirago, G.; Pesce, V.; Lezza, A.M.S.; Calvani, R.; Bossola, M.; Villani, E.R.; Landi, F.; Leeuwenburgh, C.; Bernabei, R.; Carter, C.S.; Marzetti, E. Administration of Enalapril Started Late in Life Attenuates Hypertrophy and Oxidative Stress Burden, Increases Mitochondrial Mass, and Modulates Mitochondrial Quality Control Signaling in the Rat Heart. Biomolecules 2018, 8, 177. Picca, A.; Sirago, G.; Pesce, V.; Lezza, A.M.S.; Calvani, R.; Bossola, M.; Villani, E.R.; Landi, F.; Leeuwenburgh, C.; Bernabei, R.; Carter, C.S.; Marzetti, E. Administration of Enalapril Started Late in Life Attenuates Hypertrophy and Oxidative Stress Burden, Increases Mitochondrial Mass, and Modulates Mitochondrial Quality Control Signaling in the Rat Heart. Biomolecules 2018, 8, 177.

Abstract

Mitochondrial dysfunction is relevant mechanism in cardiac aging. Here, we investigated the effects of late-life enalapril administration at non-antihypertensive dose on mitochondrial genomic stability, oxidative damage, and mitochondrial quality control (MQC) signaling in the heart of aged rats. The protein expression of selected mediators (i.e., mitochondrial antioxidant enzymes, energy metabolism, mitochondrial biogenesis, dynamics, and autophagy) was measured in old rats randomly assigned to receive enalapril (n=8) or placebo (n=8) from 24 to 27 months of age. We also assessed mitochondrial DNA (mtDNA) content, citrate synthase activity, oxidative lesions to protein and mtDNA (i.e., carbonyls and abundance of mtDNA4834 deletion), and mitochondrial transcription factor A (TFAM) binding to specific mtDNA regions. Enalapril attenuated cardiac hypertrophy and oxidative stress-derived damage (mtDNA oxidation, mtDNA4834 deletion, and protein carbonylation), while increasing mitochondrial antioxidant defenses. TFAM binding to mtDNA regions involved in replication and deletion generation was increased following enalapril administration. Increased mitochondrial mass as well as mitochondriogenesis and autophagy signaling was found in enalapril-treated rats. Late-life enalapril administration mitigates age-dependent cardiac hypertrophy and oxidative damage, while increasing mitochondrial mass and modulating MQC signaling. Further analyses are needed to conclusively establish whether enalapril may offer cardioprotection during aging.

Keywords

mitochondrial quality control, mitochondrial biogenesis, mitochondrial dynamics, mitophagy, mtDNA, TFAM binding, oxidative lesions, mtDNA damage, cardioprotection, peroxiredoxin

Subject

Biology and Life Sciences, Biochemistry and Molecular Biology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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