The mitochondria targeted antioxidant MitoQ protects against fluoroquinolone-induced oxidative stress and mitochondrial membrane damage in human Achilles tendon cells

Lowes, Damon A.; Wallace, Carol A.; Murphy, Michael P.; Webster, Nigel R.; Galley, Helen F.

doi:10.1080/10715760902736275

Cited by 67 publications

(51 citation statements)

References 31 publications

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“…Collins hopes to explore mitochondrial damage by antibiotics in other animal models. He and Murphy have also found, in lab studies 4,9 , that giving antioxidants alongside fluoroquinolones seems to mitigate the effects on mitochondria. Murphy is interested in trials to avoid mitochondrial toxicity in drugs; he owns shares in a company that aims to set some up.…”

Section: Lack Of Supportmentioning

confidence: 99%

When antibiotics turn toxic

Marchant

2018

Nature

121

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Section: Lack Of Supportmentioning

confidence: 99%

When antibiotics turn toxic

Marchant

2018

Nature

121

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“…Mitochondrial ROS production is a redox signal, mod- (Monboisse et al 1984;Bernard-Beaubois et al 1998;Shakibaei et al 2000;Reed 2000;Yuan et al 2003;Pouzaud et al 2004a;Sendzik et al 2005;Alberts et al 2008b;Lowes et al 2009;Murphy 2009;Aristilde et al 2010;Kaminski et al 2010).…”

Section: Test Agent Ultrastructural Changes Referenceunclassified

“…Concomitant use of antioxidants, such as N-acetylcysteine (Simonin et al 2000), anethole dithiolethione (Pouzaud et al 2004b), and MitoQ (Lowes et al 2009), was reported to attenuate toxic effects of FQs on tendon cells. Cotreatment with platelet rich plasma was proposed as a novel strategy to restore the reduced tenocyte viability and promote healing following FQ exposure (Zargar et al 2011).…”

Section: Test Agent Ultrastructural Changes Referencementioning

confidence: 99%

“…Mitochondria were shown to be a biological target of pefloxacin and norfloxacin in cultured rabbit Achilles tendon cells (BernardBeaubois et al 1998). Mitochondrial swelling , mitochondrial membrane damage (Lowes et al 2009), and loss of mitochondrial DNA content (Kaminski et al 2010) were reported with various FQs. An antioxidant targeted to mitochondria (MitoQ) was able to protect mitochondria membrane permeability better than a non-mitochondria targeted antioxidant, idebenone in ciprofloxacin and moxifloxacin associated oxidative stress and mitochondrial damage in cultured normal human Achilles' tendon cells (Lowes et al 2009).…”

Section: Test Agent Ultrastructural Changes Referencementioning

confidence: 99%

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Fluoroquinolone-Induced Tendinopathy: Etiology and Preventive Measures

Kaleagasioglu

Olcay

2012

Tohoku J. Exp. Med.

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Tendinopathy is a serious health problem and its etiology is not fully elucidated. Among intrinsic and extrinsic predisposing factors of tendinopathy, the impact of therapeutic agents, especially fluoroquinolone (FQ) group antibiotics, is recently being recognized. FQs are potent bactericidal agents widely used in various infectious diseases, including community acquired pneumonia and bronchitis, chronic osteomyelitis, traveler's diarrhea, typhoid fever, shigellosis, chronic bacterial prostatitis, uncomplicated cervical and urethral gonorrhea and prophylaxis of anthrax. FQs have an acceptable tolerability range. However, many lines of evidence for developing tendinitis and tendon rupture during FQ use have resulted in the addition of a warning in patient information leaflets. FQ-induced tendinopathy presents a challenge for the clinician because healing response is poor due to low metabolic rate in mature tendon tissue and tendinopathy is more likely to develop in patients who are already at high risk, such as elderly, solid organ transplant recipients and concomitant corticosteroid users. FQs become photo-activated under exposure to ultraviolet light, and this process results in formation and accumulation of intracellular reactive oxygen species (ROS). The subsequent FQ-related oxidative stress disturbs mitochondrial functions, leading to apoptosis. ROS overproduction also has direct cytotoxic effects on extracellular matrix components. Understanding the mechanisms of the FQ-associated tendinopathy may enable designing safer therapeutic strategies, hence optimization of clinical response. In this review, we evaluate multi-factorial etiology of the FQ-induced tendinopathy and discuss proposed preventive measures such as antioxidant use and protection from natural sunlight and artificial ultraviolet exposure.

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“…As an example, in vivo studies demonstrate an enhanced efficiency and an improved cellular internalization of antioxidants when coupled to chitosan derivatives (26). Finally, antioxidants targeted specifically to the mitochondria have attenuated cell injury in oxidative stress-induced disease models (71,112).…”

Section: Antioxidants As Therapy For Bpdmentioning

confidence: 99%

Developmental Regulation of Antioxidant Enzymes and Their Impact on Neonatal Lung Disease

Berkelhamer

Farrow

2014

Antioxidants & Redox Signaling

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Significance: Deficient antioxidant defenses and compromised ability to respond to oxidative stress burden the immature lung. Routine neonatal therapies can cause increased oxidative stress with subsequent injury to the premature lung. Novel therapeutic approaches to protect the premature lung are greatly needed. Recent Advances: Live cell imaging with targeted redox probes allows for the measurement of subcellular oxidative stress and for comparisons of oxidative stress across development. Comprehension of subcellular and cell-typespecific responses to oxidative stress may influence the targeting of future antioxidant therapies. Critical Issues: Challenges remain in identifying the optimal cellular targets, degree of enzyme activity, and appropriate antioxidant therapy. Further, the efficacy of delivering exogenous antioxidants to specific cell types or subcellular compartments remains under investigation. Treatment with a nonselective antioxidant could unintentionally compromise cellular function or impact cellular defense mechanisms and homeostasis. Future Directions: Genetic and/or biomarker screening may identify infants at the greatest risk for oxidative lung injury and guide the use of more selective antioxidant therapies. Novel approaches to the delivery of antioxidant enzymes may allow cell type-or cellular organelle-specific therapy. Improved comprehension of the antioxidant enzyme regulation across cell type, cell compartment, gender, and developmental stage is critical to the design and optimization of therapy.

show abstract

The mitochondria targeted antioxidant MitoQ protects against fluoroquinolone-induced oxidative stress and mitochondrial membrane damage in human Achilles tendon cells

Cited by 67 publications

References 31 publications

When antibiotics turn toxic

When antibiotics turn toxic

Fluoroquinolone-Induced Tendinopathy: Etiology and Preventive Measures

Developmental Regulation of Antioxidant Enzymes and Their Impact on Neonatal Lung Disease

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