The influence of dietary omega-3 polyunsaturated fatty acids on functional parameters of myocardial mitochondria during isoproterenol-induced heart injury

Panasiuk, Olga; Shysh, A M; Oo, Moĭbenko

doi:10.15407/fz60.01.018

Cited by 2 publications

(2 citation statements)

References 24 publications

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“…In contrast, it was shown earlier that n-3 PUFA supplementation could protect or restore mitochondrial functions e.g. against chemically-induced myocardial injury and neurodegenerative diseases in animal models [60][61][62].…”

Section: Discussionmentioning

confidence: 99%

Alpha-linolenic acid protects the developmental capacity of bovine cumulus–oocyte complexes matured under lipotoxic conditions in vitro†

Marei

Bie

Mohey-Elsaeed

et al. 2017

Biology of Reproduction

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Elevated concentrations of free fatty acids (FFAs), predominantly palmitic, stearic, and oleic acids (PSO), exert detrimental effects on oocyte developmental competence. This study examined the effects of omega-3 alpha-linolenic acid (ALA) during in vitro oocyte maturation (IVM) in the presence of PSO on subsequent embryo development and quality, and the cellular mechanisms that might be involved. Bovine cumulus-oocyte complexes (COCs) were supplemented during IVM with ALA (50 μM), PSO (425 μM), or PSO+ALA. Compared with FFA-free controls (P < 0.05), PSO increased embryo fragmentation and decreased good quality embryos on day 2 postfertilization. Day 7 blastocyst rate was also reduced. Day 8 blastocysts had lower cell counts and higher apoptosis but normal metabolic profile. In the PSO group, cumulus cell (CC) expansion was inhibited with an increased CC apoptosis while COC metabolism was not affected. Mitochondrial inner membrane potential (MMP; JC-1 staining) was reduced in the CCs and oocytes. Heat shock protein 70 (HSP70) but not glucose-regulated protein 78 kDa (GRP78, known as BiP; an endoplasmic reticulum stress marker) was upregulated in the CCs. Higher reactive oxygen species levels (DCHFDA staining) were detected in the oocytes. In contrast, adding ALA in the presence of PSO normalized embryo fragmentation, cleavage, blastocyst rates, and blastocyst quality compared to controls (P > 0.05). Combined treatment with ALA also reduced CC apoptosis, partially recovered CC expansion, abrogated the reduction in MMP in the CCs but not in the oocytes, and reduced BiP and HSP70 expression in CCs, compared with PSO only (P < 0.05). In conclusion, ALA supplementation protected oocyte developmental capacity under lipotoxic conditions mainly by protecting cumulus cell viability.

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Section: Discussionmentioning

confidence: 99%

Alpha-linolenic acid protects the developmental capacity of bovine cumulus–oocyte complexes matured under lipotoxic conditions in vitro†

Marei

Bie

Mohey-Elsaeed

et al. 2017

Biology of Reproduction

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“…Although we have no evidence of anti-oxidant and anti-inflammatory effects of melatonin and omega-3 during the acute stage of ISO effects, there was a clear subsequent benefit from both compounds, including the protection of mitochondria function. Mitochondria respiration rate was shown to be reduced after acute ISO effects but restored by omega-3 [73]. Omega-3 can incorporate into plasma membranes and potentially stabilize them to resist oxidation and confer protection against arrhythmias [67,74].…”

Section: Discussionmentioning

confidence: 99%

Antiarrhythmic Effects of Melatonin and Omega-3 Are Linked with Protection of Myocardial Cx43 Topology and Suppression of Fibrosis in Catecholamine Stressed Normotensive and Hypertensive Rats

et al. 2020

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Cardiac β-adrenergic overstimulation results in oxidative stress, hypertrophy, ischemia, lesion, and fibrosis rendering the heart vulnerable to malignant arrhythmias. We aimed to explore the anti-arrhythmic efficacy of the anti-oxidative and anti-inflammatory compounds, melatonin, and omega-3, and their mechanisms of actions in normotensive and hypertensive rats exposed to isoproterenol (ISO) induced β-adrenergic overdrive. Eight-month-old, male SHR, and Wistar rats were injected during 7 days with ISO (cumulative dose, 118 mg/kg). ISO rats were either untreated or concomitantly treated with melatonin (10 mg/kg/day) or omega-3 (Omacor, 1.68 g/kg/day) until 60 days of ISO withdrawal and compared to non-ISO controls. Findings showed that both melatonin and omega-3 increased threshold current to induce ventricular fibrillation (VF) in ISO rats regardless of the strain. Prolonged treatment with these compounds resulted in significant suppression of ISO-induced extracellular matrix alterations, as indicated by reduced areas of diffuse fibrosis and decline of hydroxyproline, collagen-1, SMAD2/3, and TGF-β1 protein levels. Importantly, the highly pro-arrhythmic ISO-induced disordered cardiomyocyte distribution of electrical coupling protein, connexin-43 (Cx43), and its remodeling (lateralization) were significantly attenuated by melatonin and omega-3 in Wistar as well as SHR hearts. In parallel, both compounds prevented the post-ISO-related increase in Cx43 variant phosphorylated at serine 368 along with PKCε, which are known to modulate Cx43 remodeling. Melatonin and omega-3 increased SOD1 or SOD2 protein levels in ISO-exposed rats of both strains. Altogether, the results indicate that anti-arrhythmic effects of melatonin and omega-3 might be attributed to the protection of myocardial Cx43 topology and suppression of fibrosis in the setting of oxidative stress induced by catecholamine overdrive in normotensive and hypertensive rats.

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The influence of dietary omega-3 polyunsaturated fatty acids on functional parameters of myocardial mitochondria during isoproterenol-induced heart injury

Cited by 2 publications

References 24 publications

Alpha-linolenic acid protects the developmental capacity of bovine cumulus–oocyte complexes matured under lipotoxic conditions in vitro†

Alpha-linolenic acid protects the developmental capacity of bovine cumulus–oocyte complexes matured under lipotoxic conditions in vitro†

Antiarrhythmic Effects of Melatonin and Omega-3 Are Linked with Protection of Myocardial Cx43 Topology and Suppression of Fibrosis in Catecholamine Stressed Normotensive and Hypertensive Rats

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