Mitochondria-Targeted Antioxidant Peptides

Rocha, Milagros; Hernández‐Mijares, Antonio; Garcia-Malpartida, Katherinne; Bañuls, Celia; Bellod, Lorena; Víctor, Víctor M.

doi:10.2174/138161210793292519

Cited by 80 publications

(60 citation statements)

References 63 publications

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“…SS peptides scavenge H2O2 and peroxynitrite inhibits lipid peroxidation. They can also inhibit the decline of MPT and cytochrome c release, thus preventing oxidant-induced cell death [64] . Although the delivery of antioxidants may protect mitochondria from oxidative stress caused by a variety of insults, the area of mitochondria-specific delivery of drugs is still in its infancy.…”

Section: Future Perspectives Of Mitochondrial Pharmaceutics In Cardiomentioning

confidence: 99%

Mitochondria-targeted agents: Future perspectives of mitochondrial pharmaceutics in cardiovascular diseases

Ajith

Jayakumar

2014

WJC

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Mitochondria are one of the major sites for the generation of reactive oxygen species (ROS) as an undesirable side product of oxidative energy metabolism. Damaged mitochondria can augment the generation of ROS. Dysfunction of mitochondria increase the risk for a large number of human diseases, including cardiovascular diseases (CVDs). Heart failure (HF) following ischemic heart disease, infantile cardiomyopathy and cardiac hypertrophy associated with left ventricular dilations are some of the CVDs in which the role of mitochondrial oxidative stress has been reported. Advances in mitochondrial research during the last decade focused on the preservation of its function in the myocardium, which is vital for the cellular energy production. Experimental and clinical trials have been conducted using mitochondria-targeted molecules like: MnSOD mimetics, such as EUK-8, EUK-134 and MitoSOD; choline esters of glutathione and N -acetyl-L-cysteine; triphenylphosphonium ligated vitamin E, lipoic acid, plastoquinone and mitoCoQ10; and Szeto-Schiller (SS)-peptides (SS-02 and SS-31). Although many results are inconclusive, some of the findings, especially on CoQ10, are worthwhile. This review summarizes the role of mitochondria-targeted delivery of agents and their consequences in the control of HF.

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Section: Future Perspectives Of Mitochondrial Pharmaceutics In Cardiomentioning

confidence: 99%

Mitochondria-targeted agents: Future perspectives of mitochondrial pharmaceutics in cardiovascular diseases

Ajith

Jayakumar

2014

WJC

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“…4 Oxidative damage to mitochondria is a critical event in oxidative cell damage, and mitochondrial ROS should be a primary target for drug development. 5 A novel, water-soluble mitochondria-targeted peptide (MTP) was designed by Hazel H.Szeto and Peter W. Schiller, named MTP131 or SS-31, 6 and SPI 20 was another peptide in this series, which could scavenge ROS and inhibit lipid peroxidation in vitro. In addition, MTP131 and SPI 20 could reduce mitochondrial ROS, and prevent mitochondrial swelling.…”

Section: Introductionmentioning

confidence: 99%

Mitochondria-targeted peptides prevent on contrast-induced acute kidney injury in the rats with hypercholesterolemia

et al. 2013

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Objective: The objective of this study is to evaluate the effect and mechanism of mitochondriatargeted peptides (MTP131 and SPI20) on contrast-induced acute kidney injury (CI-AKI) in rats with hypercholesterolemia. Method: Forty SD rats were randomly divided into normal diet group (NN, n ¼ 8) and high cholesterol supplemented dietary group (HN, n ¼ 32). At the end of 8 weeks, the group HN was divided into four subgroups. All Rats were given injection of either diatrizoate (10 mL/kg) or equal volume of normal saline, the rats pretreated with MTP131 or SPI20 were given injection with MTP131 or SPI 20 (3 mg/kg) by peritoneal cavity for 3 times. Blood, urine and renal tissue samples were prepared to determine biochemical parameters. The renal pathological changes were evaluated by hematoxylin and eosin staining and scored semiquantitatively, The protein expression of renal NOX4 was also measured by Western blotting. Results: In diatrizoate-injected rats, Serum creatinine (Scr), fractional excretion of sodium (FeNa%), fractional excretion of potassium (FeK%), pathological scores, renal malondialdehyde (MDA) content, the NADPH oxidase activity and the expression of NOX4 in kidney tissue were significantly increased (p50.01). In the groups pretreated with MTP131 or SPI20, the levels of Scr, FeNa%, FeK%, MDA content and NADPH oxidase activity in renal tissue decreased (p50.01), the levels of renal super oxygen dehydrogenises and ATPase activity increased (p50.01). The renal injuries induced by contrast media (CM) were alleviated. Conclusion: MTP131 and SPI20 might protect acute kidney injury induced by CM in rats with hypercholesterolemia.

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“…In summary, increasing the antioxidant capacity, particularly in the mitochondrial compartment, represents a potential therapy whose pharmaceutical viability depends on the employment of small-molecule antioxidants [40,41,[52][53][54][55][56][57][58]. However, small-molecule antioxidants spread all over the body, with only a small fraction being consumed by the mitochondria.…”

Section: Antioxidantsmentioning

confidence: 99%

Mitochondrial Dysfunction and Antioxidant Therapy in Sepsis

Rocha¹,

Herance

Rovira³

et al. 2012

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Sepsis and septic shock are the major causes of death in intensive care units. Oxidative damage to mitochondria is involved in the development of organ dysfunction associated with sepsis. This syndrome is caused by an excessive defensive and inflammatory response characterised by a massive increases of reactive oxygen species (ROS), nitric oxide (NO) and inflammatory cytokines. Under normal circumstances, complex interacting antioxidant defense systems control oxidative stress within mitochondria The consequences of sepsis is a systemic damage to the vascular endothelium, impaired tissue and a compromised whole body respiration, antioxidant depletion and mitochondrial respiratory dysfunction with diminished levels of ATP and O2 consumption. In general, ROS are essential to the functions of cells and particularly immune cells, but adequate levels of antioxidant defenses are required to protect against the harmful effects of excessive ROS production. This review considers the process of sepsis from a mitochondrial perspective, discussing strategies for the targeted delivery of antioxidants to mitochondria. We will provide a summary of the following areas: the cellular metabolism of ROS and its role in pathophysiological processes such as sepsis; currently available antioxidants and possible reasons for their efficacy and inefficacy in ameliorating oxidative stress-mediated diseases; and recent developments in mitochondria-targeted antioxidants and the future implications for such approaches in patients.

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Mitochondria-Targeted Antioxidant Peptides

Cited by 80 publications

References 63 publications

Mitochondria-targeted agents: Future perspectives of mitochondrial pharmaceutics in cardiovascular diseases

Mitochondria-targeted agents: Future perspectives of mitochondrial pharmaceutics in cardiovascular diseases

Mitochondria-targeted peptides prevent on contrast-induced acute kidney injury in the rats with hypercholesterolemia

Mitochondrial Dysfunction and Antioxidant Therapy in Sepsis

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