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Comparative Evaluation of Mitochondrial Antioxidants in Oral Potentially Malignant Disorders.

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Comparative Evaluation of Mitochondrial Antioxidants in Oral Potentially Malignant Disorders.

Auteurs : Sumita Banerjee ; Saikat Mukherjee ; Sanjib Mitra ; Pallav Singhal

Source :

RBID : pubmed:32378537

Abstract

Various endogenous mitochondria-associated antioxidants protect mitochondria from oxidative stresses such as Superoxide Dismutase 2 (SOD2), Catalase, Glutaredoxin 2 (GLRX2), educed Glutathione (GSH), Glutathione Peroxidase (GPx), and Thioredoxin 2 (TXN2). They protect mitochondria from Reactive Oxygen Species (ROS). Excess ROS causes mitochondrial DNA damage and respiratory chain dysfunction leading to carcinogenesis. In an earlier study we found complex alterations of mitochondrial antioxidants in different stages of oral squamous cell carcinoma. Here, we profiled mitochondrial antioxidants in different oral potentially malignant disorders such as oral leukoplakia (OL), oral lichen planus (OLP), and oral submucous fibrosis (OSMF). Mitochondria was prepared from oral tissues from OL, OLP, and OSMF patients. Biochemical assays and immunoblotting were performed to investigate expression of various mitochondrial antioxidants. Catalase was expressed as Control> OL > OSMF > OLP. GLRX 2 was expressed as OLP> OL >Control >OSMF. GPX1 and GPX4 were expressed as Control >OSMF> OLP > OL. GSH increased in OL and OSMP, but decreased in OLP. SOD2 was expressed as Control >OSMF> OLP > OL. PRX3 was expressed as OL > OLP > OSMF > Control. TXN2 expression was nearly the same in all groups except OL, which showed elevated expression. We conclude that endogenous mitochondria-associated antioxidants show different levels of expressions in various oral potentially malignant disorders.

DOI: 10.2739/kurumemedj.MS661009
PubMed: 32378537


Affiliations:


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<div type="abstract" xml:lang="en">Various endogenous mitochondria-associated antioxidants protect mitochondria from oxidative stresses such as Superoxide Dismutase 2 (SOD2), Catalase, Glutaredoxin 2 (GLRX2), educed Glutathione (GSH), Glutathione Peroxidase (GPx), and Thioredoxin 2 (TXN2). They protect mitochondria from Reactive Oxygen Species (ROS). Excess ROS causes mitochondrial DNA damage and respiratory chain dysfunction leading to carcinogenesis. In an earlier study we found complex alterations of mitochondrial antioxidants in different stages of oral squamous cell carcinoma. Here, we profiled mitochondrial antioxidants in different oral potentially malignant disorders such as oral leukoplakia (OL), oral lichen planus (OLP), and oral submucous fibrosis (OSMF). Mitochondria was prepared from oral tissues from OL, OLP, and OSMF patients. Biochemical assays and immunoblotting were performed to investigate expression of various mitochondrial antioxidants. Catalase was expressed as Control> OL > OSMF > OLP. GLRX 2 was expressed as OLP> OL >Control >OSMF. GPX1 and GPX4 were expressed as Control >OSMF> OLP > OL. GSH increased in OL and OSMP, but decreased in OLP. SOD2 was expressed as Control >OSMF> OLP > OL. PRX3 was expressed as OL > OLP > OSMF > Control. TXN2 expression was nearly the same in all groups except OL, which showed elevated expression. We conclude that endogenous mitochondria-associated antioxidants show different levels of expressions in various oral potentially malignant disorders.</div>
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