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Lymphocyte micronuclei frequencies in skin, haematological, prostate, colorectal and esophageal cancer cases: A systematic review and meta-analysis

Dhillon VS, Deo P, Bonassi S, Fenech M

Mutat Res Rev Mutat Res, 2021;787:108372.
PMID: 34083057 DOI: 10.1016/j.mrrev.2021.108372

Micronucleus (MN) assay has been widely used as a biomarker of DNA damage, chromosomal instability, cancer risk and accelerated aging in many epidemiological studies. In this narrative review and meta-analysis we assessed the association between lymphocyte micronuclei (MNi) and cancers of the skin, blood, digestive tract, and prostate. The review identified nineteen studies with 717 disease subjects and 782 controls. Significant increases in MRi for MNi were observed in the following groups: subjects with blood cancer (MRi = 3.98; 95 % CI: 1.98-7.99; p = 0.000) and colorectal cancer (excluding IBD) (MRi = 2.69; 95 % CI: 1.82-3.98, p DNA damage and chromosomal instability in people with haematological or colorectal cancers. However, the MRi for lymphocyte MNi in subjects with cancers of skin, prostate, esophagus was not significantly increased. More case-control and prospective studies are warranted to further verify the observed trends and to better understand the role of lymphocyte MNi as a biomarker of cancer risk in blood, skin, digestive tract and prostate.

Matched MeSH terms: DNA Damage/physiology
Increase in maternal adiposity and poor lipid profile is associated with oxidative stress markers during pregnancy

Loy SL, KNS S, JM HJ

Prev Med, 2013;57 Suppl:S41-4.
PMID: 23219759 DOI: 10.1016/j.ypmed.2012.11.021

This study aimed to evaluate changes in maternal adiposity and lipid profile and to correlate these parameters with Deoxyribonucleic acid (DNA) damage and total antioxidant capacity (TAC) levels among pregnant women.

Matched MeSH terms: DNA Damage/physiology
Fulltext Impaired coronary metabolic dilation in the metabolic syndrome is linked to mitochondrial dysfunction and mitochondrial DNA damage

Guarini G, Kiyooka T, Ohanyan V, Pung YF, Marzilli M, Chen YR, et al.

Basic Res Cardiol, 2016 May;111(3):29.
PMID: 27040114 DOI: 10.1007/s00395-016-0547-4

Mitochondrial dysfunction in obesity and diabetes can be caused by excessive production of free radicals, which can damage mitochondrial DNA. Because mitochondrial DNA plays a key role in the production of ATP necessary for cardiac work, we hypothesized that mitochondrial dysfunction, induced by mitochondrial DNA damage, uncouples coronary blood flow from cardiac work. Myocardial blood flow (contrast echocardiography) was measured in Zucker lean (ZLN) and obese fatty (ZOF) rats during increased cardiac metabolism (product of heart rate and arterial pressure, i.v. norepinephrine). In ZLN increased metabolism augmented coronary blood flow, but in ZOF metabolic hyperemia was attenuated. Mitochondrial respiration was impaired and ROS production was greater in ZOF than ZLN. These were associated with mitochondrial DNA (mtDNA) damage in ZOF. To determine if coronary metabolic dilation, the hyperemic response induced by heightened cardiac metabolism, is linked to mitochondrial function we introduced recombinant proteins (intravenously or intraperitoneally) in ZLN and ZOF to fragment or repair mtDNA, respectively. Repair of mtDNA damage restored mitochondrial function and metabolic dilation, and reduced ROS production in ZOF; whereas induction of mtDNA damage in ZLN reduced mitochondrial function, increased ROS production, and attenuated metabolic dilation. Adequate metabolic dilation was also associated with the extracellular release of ADP, ATP, and H2O2 by cardiac myocytes; whereas myocytes from rats with impaired dilation released only H2O2. In conclusion, our results suggest that mitochondrial function plays a seminal role in connecting myocardial blood flow to metabolism, and integrity of mtDNA is central to this process.

Matched MeSH terms: DNA Damage/physiology
Hot water extract of Chlorella vulgaris induced DNA damage and apoptosis

Yusof YA, Saad SM, Makpol S, Shamaan NA, Ngah WZ

Clinics (Sao Paulo), 2010;65(12):1371-7.
PMID: 21340229

OBJECTIVES: The aim of this study was to determine the antiproliferative and apoptotic effects of hot water extracts of Chlorella vulgaris on hepatoma cell line HepG2.
INTRODUCTION: The search for food and spices that can induce apoptosis in cancer cells has been a major study interest in the last decade. Chlorella vulgaris, a unicellular green algae, has been reported to have antioxidant and anti-cancer properties. However, its chemopreventive effects in inhibiting the growth of cancer cells have not been studied in great detail.
METHODS: HepG2 liver cancer cells and WRL68 normal liver cells were treated with various concentrations (0-4 mg/ml) of hot water extract of C. vulgaris after 24 hours incubation. Apoptosis rate was evaluated by TUNEL assay while DNA damage was assessed by Comet assay. Apoptosis proteins were evaluated by Western blot analysis.
RESULTS: Chlorella vulgaris decreased the number of viable HepG2 cells in a dose dependent manner (p < 0.05), with an IC50 of 1.6 mg/ml. DNA damage as measured by Comet assay was increased in HepG2 cells at all concentrations of Chlorella vulgaris tested. Evaluation of apoptosis by TUNEL assay showed that Chlorella vulgaris induced a higher apoptotic rate (70%) in HepG2 cells compared to normal liver cells, WRL68 (15%). Western blot analysis showed increased expression of pro-apoptotic proteins P53, Bax and caspase-3 in the HepG2 cells compared to normal liver cells WRL68, and decreased expression of the anti-apoptotic protein Bcl-2.
CONCLUSIONS: Chlorella vulgaris may have anti-cancer effects by inducing apoptosis signaling cascades via an increased expression of P53, Bax and caspase-3 proteins and through a reduction of Bcl-2 protein, which subsequently lead to increased DNA damage and apoptosis.

Matched MeSH terms: DNA Damage/physiology*
Associations between prenatal nicotine exposure, oxidative stress, and postpartum visceral fat

Loy SL, Jan Mohamed HJ

Women Health, 2014;54(2):145-60.
PMID: 24329183 DOI: 10.1080/03630242.2013.870632

This study aimed to examine the associations among prenatal nicotine exposure, oxidative stress, and postpartum visceral fat among women exposed to secondhand smoke (SHS). The study was conducted in Kelantan, Malaysia, from April 2010 to December 2012. Blood samples were collected in the second and third trimesters from 135 healthy pregnant women who were followed-up at delivery, 2 months, 6 months and 12 months postpartum. Maternal hair nicotine and oxidative stress markers during pregnancy were measured. Visceral fat was assessed by bioelectrical impedance. Multiple linear regression analysis revealed that maternal hair nicotine concentration was associated with increased DNA damage (tail moment: β=0.580, p=0.001) and decreased glutathione peroxidase (β=-12.100; p=0.009) in the second trimester of pregnancy. Increased DNA damage, protein oxidation and total antioxidant capacity in the second trimester were associated with 2, 6, and 12 months postpartum visceral fat. No direct association was found between prenatal hair nicotine level and postpartum visceral fat; however, these results suggest that any relation of SHS to visceral adiposity may be indirect, mediated via enhanced oxidative stress.

Matched MeSH terms: DNA Damage/physiology