ABSTRACT
The protective roles of α-lipoic acid in the rat model of mitochondrial DNA(mtDNA)4834bp deletion in inner ear were investigated.Forty female Wistar rats at 4 weeks of age were divided into four groups: group A(D-galactose group,n= 10),group B(D-galactose+α-lipoic acid group,n=10),group C(α-lipoic acid group,n=10),and group D(control group,n=10).Auditory brainstem response(ABR)was used to detect the hearing threshold.Colorimetry was used to analyze activity of superoxide dismutase(SOD)and concentration of malondialdehyde(MDA).The percentage of mtDNA4834bp deletion in inner ear was identified by real-time PCR.There was no significant difference in ABR threshold shift among all groups.The percentage ofmtDNA4834bp deletion in group A was higher than that in other groups,but there was no significant difference in percentage of mtDNA4834bp deletion among groups B,C,and D.The activity of SOD in group A was lower than that in other groups.The concentration of MDA in group A was higher than that in other groups.It was concluded that there was no significant heating loss when the percentage of mtDNA4834bp deletion was lower than 12.5%.α-Lipoic acid could prevent the reactive oxygen species(ROS)-induced mtDNA4834bp deletion in inner ear of rats.
ABSTRACT
Recently, efforts have been focused on mitochondrial DNA changes and their relation to human cancers. Among them, a 4977 bp deletion of mitochondrial DNA, named "common deletion", has been investigated in several types of tumors, with inconsistent results. In this study, we investigated the presence of the common deletion in tissues from 25 breast, 25 colorectal and 50 thyroid tumors and in the adjacent healthy tissues from Turkish patients. Samples from healthy volunteers were also evaluated for comparison. Two PCR-based methods were used for the detection of the common deletion. First, two pairs of primers were used to amplify wild-type and deleted mtDNA. Then, a highly sensitive nested-PCR was performed, to determine low amounts of deleted genomes. By the first method, wild-type mtDNAs were observed in all samples, but a deletion was observed in only six thyroid samples, by using the nested-PCR method. In conclusion, the mitochondrial common deletion was very rare in our study group and did not appear to be not related with cancer.
ABSTRACT
OBJECTIVES: Controversial arguments exists on both the case for and against on the accumulation of mitochondrial DNA (mtDNA) deletion in association to tissue and age. The debate continues as to whether this mutation is a major contributor to the phenotypic expression of aging and common degenerative diseases or simply a clinical insignificant epiphenomenon. The objective of this study was to determine whether the accumulation of mtDNA deletion is correlated with age-related and tissue-specific variation. MATERIALS AND METHODS: One hundred and fifty-seven tissues from blood, ovary, uterine muscle, and abdominal muscle were obtained from patients ranging in age from 31~60 years. After reviewing the clinical reports, patients with mitochondrial disorder were excluded from this study. The tissues were obtained at gynecological surgeries with the consent of the patient. Total DNA isolated from blood, ovary, uterine muscle, and abdominal muscle was amplified by two rounds of PCR using two pairs of primers corresponding to positions 8225-8247 (sense), 13551-13574 (antisense) for the area around deleted mtDNA and 8421-8440 (sense), 13520-13501 (antisense) for nested PCR product. A statistical analysis was performed by c2-test. RESULTS: About 0% of blood, 94.8% of ovary, 71.4% of uterine muscle, and 86.1% abdominal muscle harbored mtDNA deletion. When we examined the proportion of deleted mtDNA according to age deletion rate was 90% of ovary, 63.6% of uterine muscle, 77.7% of abdominal muscle in thirties and 100% of all tissue in fifties. CONCLUSION: The findings of this study suggest that the mtDNA deletion is varied in tissue-specific pattern and increases with aging.