Accumulation of mitochondrial DNA deletions in the malignant prostate of patients of different ages

Jessie, Benjamin C.; Sun, Carrie; Irons, Hillary R.; Marshall, Fray F.; Wallace, Douglas C.; Petros, John A.

doi:10.1016/s0531-5565(01)00153-x

Cited by 55 publications

(33 citation statements)

References 10 publications

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“…It is possible that the mtDNA deletion may cause tissue aging and increased cancer risk. Jessie et al (Jessie et al 2001) suggest that mtDNA deletions are not only a marker for aging, but also a cause of aging and cancer risk in the tissues.…”

Section: Discussionmentioning

confidence: 99%

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

Çanakçı

Tatar

et al. 2009

Arch. Immunol. Ther. Exp.

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Introduction: Oxidative stress may contribute to the pathogenesis of periodontitis. However, the detailed molecular mechanism remains unclear. Both 8-hydroxydeoxyguanosine (8-OHdG) and mitochondrial DNA (mtDNA) deletion have been reported as early oxidative DNA damage markers. In this study, 8-OHdG levels in saliva and mtDNA deletions in gingival tissue of patients with chronic periodontitis (CP) were evaluated. Materials and Methods: Gingival tissue and whole saliva samples were collected from 32 patients with CP and 32 healthy control subjects. To determine the clinical condition of each subject, the plaque index, gingival index, clinical attachment level (CAL), and probing depth (PD) were measured. Using the ELISA and polymerase chain reaction methods, the salivary 8-OHdG levels and the 7.4-kbp and 5-kbp mtDNA deletions were examined. Results: The 5-kbp mtDNA deletion was detected in 20 of the 32 periodontitis patients (62.5%), but was not detected in the healthy controls. The mean value of 8-OHdG in the saliva of the periodontitis patients with deleted mtDNA was significantly higher than in the patients with non-deleted mtDNA (p<0.01). Also, significant correlation was found between the occurrence of the 5-kbp mtDNA deletion and salivary 8-OHdG levels (p<0.01). Similar correlations were detected between salivary 8-OHdG levels and age, PD, and CAL (p<0.01, p<0.05). Conclusion: Increased oxidative stress may lead to premature oxidative DNA damage in the gingival tissue of periodontitis patients and the salivary 8-OHdG level may signify premature oxidative mtDNA damage in diseased gingival tissue.

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Section: Discussionmentioning

confidence: 99%

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

Çanakçı

Tatar

et al. 2009

Arch. Immunol. Ther. Exp.

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“…Prostate cancer is associated with aging and mtDNA depletion and deletion mutations accumulate with age in many tissues of the body, suggesting a potential link. Heteroplasmic large deletion mutant mtDNA is very common in prostate cancer (Jessie et al, 2001). We investigated the roles of mtDNA by using human androgendependent prostate cancer cell line LNCaP and androgen-independent C4-2, sub clone derived by inoculation of LNCaP into castrated mice (Wu et al, 1994), mtDNA deficient cells derived from LNCaP, and cybrids which has nuclear DNA from LNCaP with healthy mtDNA.…”

Section: Mtdna Determines Androgen Dependence In Prostate Cancer Cellmentioning

confidence: 99%

Regulation of mitochondrial DNA content and cancer

Higuchi

2007

Mitochondrion

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Enzymatic activities of the proteins encoded in nuclear genome are regulated by transcriptional, translational and post-transcriptional level. Enzymatic activities of proteins encoded in mitochondrial DNA (mtDNA) have been considered to be regulated by the same steps although detailed mechanisms might differ. However, dynamic change of the number of mtDNA, from some hundred to more than ten thousand, should be considered as another novel mechanism to regulate mtDNA-encoded proteins. Recently, we showed the connection of mtDNA depletion and deletion to cancer progression (Higuchi et al., 2006). This review focuses and describes the possible connections of the mitochondrial DNA depletion and deletion to cancer.

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“…Additionally, the occurrence of this deletion was four times greater in oral tissues of individuals who chewed areca nut, a major risk factor for oral and esophageal cancer, and the deletion was also induced in neuronal cells exposed to the mutagen ethidium bromide (12,13). Furthermore, major mtDNA deletions have been identified in human prostate and breast cancers as well as numerous smaller deletions in a variety of other tumors (14)(15)(16)). …”

Section: Introductionmentioning

confidence: 99%

Arsenic Induced Mitochondrial DNA Damage and Altered Mitochondrial Oxidative Function: Implications for Genotoxic Mechanisms in Mammalian Cells

Partridge¹,

Huang

Hernandez-Rosa

et al. 2007

Cancer Research

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Arsenic is a well-established human carcinogen that is chronically consumed in drinking water by millions of people worldwide. Recent evidence has suggested that arsenic is a genotoxic carcinogen. Furthermore, we have shown that mitochondria mediate the mutagenic effects of arsenic in mammalian cells, as arsenic did not induce nuclear mutations in mitochondrial DNA (mtDNA)-depleted cells. Using the human-hamster hybrid A L cells, we show here that arsenic alters mitochondrial function by decreasing cytochrome c oxidase function and oxygen consumption but increasing citrate synthase function. These alterations correlated with depletion in mtDNA copy number and increase in large heteroplasmic mtDNA deletions. In addition, mtDNA isolated periodically from cultures treated continuously with arsenic did not consistently display the same deletion pattern, indicating that the mitochondrial genome was subjected to repeated and continuous damage. These data support the theory that the mitochondria, and particularly mtDNA, are important targets of the mutagenic effects of arsenic in mammalian cells. [Cancer Res 2007;67(11):5239-47]

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Accumulation of mitochondrial DNA deletions in the malignant prostate of patients of different ages

Cited by 55 publications

References 10 publications

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

Regulation of mitochondrial DNA content and cancer

Arsenic Induced Mitochondrial DNA Damage and Altered Mitochondrial Oxidative Function: Implications for Genotoxic Mechanisms in Mammalian Cells

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