scholarly journals Oxidative stress induces mitochondrial dysfunction in a subset of autistic lymphoblastoid cell lines

2014 ◽  
Vol 4 (4) ◽  
pp. e377-e377 ◽  
Author(s):  
S Rose ◽  
R E Frye ◽  
J Slattery ◽  
R Wynne ◽  
M Tippett ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cell Lines ◽  
Lymphoblastoid Cell Lines

scholarly journals Increased Susceptibility to Ethylmercury-Induced Mitochondrial Dysfunction in a Subset of Autism Lymphoblastoid Cell Lines

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Shannon Rose ◽  
Rebecca Wynne ◽  
Richard E. Frye ◽  
Stepan Melnyk ◽  
S. Jill James
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cell Lines ◽  
Autism Spectrum ◽  
Reserve Capacity ◽  
Flux Analysis ◽  
Lymphoblastoid Cell Lines ◽  
Extracellular Flux ◽  
Respiratory Parameters ◽  
Increased Risk

The association of autism spectrum disorders with oxidative stress, redox imbalance, and mitochondrial dysfunction has become increasingly recognized. In this study, extracellular flux analysis was used to compare mitochondrial respiration in lymphoblastoid cell lines (LCLs) from individuals with autism and unaffected controls exposed to ethylmercury, an environmental toxin known to deplete glutathione and induce oxidative stress and mitochondrial dysfunction. We also tested whether pretreating the autism LCLs with N-acetyl cysteine (NAC) to increase glutathione concentrations conferred protection from ethylmercury. Examination of 16 autism/control LCL pairs revealed that a subgroup (31%) of autism LCLs exhibited a greater reduction in ATP-linked respiration, maximal respiratory capacity, and reserve capacity when exposed to ethylmercury, compared to control LCLs. These respiratory parameters were significantly elevated at baseline in the ethylmercury-sensitive autism subgroup as compared to control LCLs. NAC pretreatment of the sensitive subgroup reduced (normalized) baseline respiratory parameters and blunted the exaggerated ethylmercury-induced reserve capacity depletion. These findings suggest that the epidemiological link between environmental mercury exposure and an increased risk of developing autism may be mediated through mitochondrial dysfunction and support the notion that a subset of individuals with autism may be vulnerable to environmental influences with detrimental effects on development through mitochondrial dysfunction.

scholarly journals Erratum: Oxidative stress induces mitochondrial dysfunction in a subset of autistic lymphoblastoid cell lines

2015 ◽  
Vol 5 (3) ◽  
pp. e526-e526 ◽  
Author(s):  
S Rose ◽  
R E Frye ◽  
J Slattery ◽  
R Wynne ◽  
M Tippett ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cell Lines ◽  
Lymphoblastoid Cell Lines

scholarly journals Oxidative Stress Induces Mitochondrial Dysfunction in a Subset of Autism Lymphoblastoid Cell Lines in a Well-Matched Case Control Cohort

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e85436 ◽  
Author(s):  
Shannon Rose ◽  
Richard E. Frye ◽  
John Slattery ◽  
Rebecca Wynne ◽  
Marie Tippett ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cell Lines ◽  
Case Control ◽  
Lymphoblastoid Cell Lines ◽  
Control Cohort ◽  
Matched Case

scholarly journals Mitochondria-Targeted Antioxidants for Treatment of Hearing Loss: A Systematic Review

Antioxidants ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 109 ◽  
Author(s):  
Chisato Fujimoto ◽  
Tatsuya Yamasoba
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Mitochondrial Dysfunction ◽  
Cell Lines ◽  
Mitochondrial Gene ◽  
Protective Effects ◽  
Drug Induced ◽  
Age Related ◽  
Cochlear Damage ◽  
Age Related Hearing Loss

Mitochondrial dysfunction is associated with the etiologies of sensorineural hearing loss, such as age-related hearing loss, noise- and ototoxic drug-induced hearing loss, as well as hearing loss due to mitochondrial gene mutation. Mitochondria are the main sources of reactive oxygen species (ROS) and ROS-induced oxidative stress is involved in cochlear damage. Moreover, the release of ROS causes further damage to mitochondrial components. Antioxidants are thought to counteract the deleterious effects of ROS and thus, may be effective for the treatment of oxidative stress-related diseases. The administration of mitochondria-targeted antioxidants is one of the drug delivery systems targeted to mitochondria. Mitochondria-targeted antioxidants are expected to help in the prevention and/or treatment of diseases associated with mitochondrial dysfunction. Of the various mitochondria-targeted antioxidants, the protective effects of MitoQ and SkQR1 against ototoxicity have been previously evaluated in animal models and/or mouse auditory cell lines. MitoQ protects against both gentamicin- and cisplatin-induced ototoxicity. SkQR1 also provides auditory protective effects against gentamicin-induced ototoxicity. On the other hand, decreasing effect of MitoQ on gentamicin-induced cell apoptosis in auditory cell lines has been controversial. No clinical studies have been reported for otoprotection using mitochondrial-targeted antioxidants. High-quality clinical trials are required to reveal the therapeutic effect of mitochondria-targeted antioxidants in terms of otoprotection in patients.

Epstein-Barr virus induces an oxidative stress during the early stages of infection in B lymphocytes, epithelial, and lymphoblastoid cell lines

2008 ◽  
Vol 313 (1-2) ◽  
pp. 179-186 ◽  
Author(s):  
Saloua Lassoued ◽  
Randa Ben Ameur ◽  
Wajdi Ayadi ◽  
Bochra Gargouri ◽  
Riadh Ben Mansour ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
B Lymphocytes ◽  
Cell Lines ◽  
Epstein Barr Virus ◽  
Lymphoblastoid Cell Lines ◽  
Barr Virus ◽  
Early Stages ◽  
Epstein Barr

Microsatellite polymorphism in heme oxygenase-1 gene promoter is associated with susceptibility to oxidant-induced apoptosis in lymphoblastoid cell lines

Blood ◽  
2003 ◽  
Vol 102 (5) ◽  
pp. 1619-1621 ◽  
Author(s):  
Hisao Hirai ◽  
Hiroshi Kubo ◽  
Mutsuo Yamaya ◽  
Katsutoshi Nakayama ◽  
Muneo Numasaki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Lines ◽  
Heme Oxygenase ◽  
Length Polymorphism ◽  
Pulmonary Emphysema ◽  
Gene Promoter ◽  
Heme Oxygenase 1 ◽  
Lymphoblastoid Cell Lines ◽  
Flanking Region ◽  
Induced Apoptosis

AbstractHeme oxygenase-1 (HO-1) confers cytoprotection against oxidative stress. A (GT)n dinucleotide repeat in the 5′-flanking region of human HO-1 gene shows length polymorphism, which was classified into S (< 27 GT), M (27-32 GT), and L alleles (≥ 33 GT). Polymorphism in the HO-1 gene promoter was shown to be associated with susceptibility to pulmonary emphysema and restenosis after angioplasty. However, the biologic mechanism underlying these associations is still unclear. To examine this issue, we established lymphoblastoid cell lines (LCLs) from subjects possessing S/S or L/L genotypes. HO-1 mRNA expressions and HO activities induced by oxidative stress were significantly higher in LCLs with S/S than those with L/L. Furthermore, LCLs with S/S were significantly more resistant to oxidant-induced apoptosis than those with L/L. These findings suggested that the polymorphism of the HO-1 gene is associated with the strength of antiapoptotic effects of HO-1, resulting in an association with susceptibility to oxidative stress–mediated diseases.

scholarly journals Oxidative Stress Challenge Uncovers Trichloroacetaldehyde Hydrate-Induced Mitoplasticity in Autistic and Control Lymphoblastoid Cell Lines

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Richard Eugene Frye ◽  
Shannon Rose ◽  
Rebecca Wynne ◽  
Sirish C. Bennuri ◽  
Sarah Blossom ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Lines ◽  
Lymphoblastoid Cell Lines ◽  
And Control
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