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Aims: To test if the level of oxidative stress is different in women with overweight and with metabolic syndrome. Study Design: Cross-sectional. Place and Duration of Study: Endocrinology Clinic of the Botucatu Medical School-UNESP, between March 2013 and March 2014. Methodology: Eighty women (31.15 ± 7.91 years old) attended at the Endocrinology Clinic of the Botucatu Medical School-UNESP composed this study. According to the body mass index (BMI) Original Research Article Talon et al.; AJARR, 13(2): 43-52, 2020; Article no.AJARR.60210 44 they were divided in 3 groups: Group 1 (G1, n=36 eutrophic); Group 2 (G2, n=21 overweight) and Group 3 (G3, n=23 women with MS-Metabolic syndrome). It was evaluated: dietary intake of macro and micronutrients dietary; antioxidant capacity (HAC) of plasma and levels of malondialdehyde (MDA); carotenoids, retinol and α-tocopherol in peripheral lymphocytes and the comet assay. Results: Damage to DNA, oxidized purines and the levels of MDA didn't differ between women with overweight and with metabolic syndrome but they are higher than those in the control group. Correlation was positive for BMI and waist circumference (WC) with damage to DNA. Linear regression showed that higher consumption of protein and sodium is related to damage to DNA and both carotenoids and omega-3 are protectors. Conclusion: Damage to DNA occurs independent of overweight or obesity and WC could be a predictor for damage to DNA.
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Asian Journal of Advanced Research and Reports
13(2): 43-52, 2020; Article no.AJARR.60210
ISSN: 2582-3248
Increased BMI and Waist Circumference are Related
to Increased DNA Damage in Women with
Overweight and Metabolic Syndrome
Lidiana de Camargo Talon1, Ana Paula Costa Rodrigues Ferraz1,
Damiana Tortolero Pierine1, Igor Otávio Minatel2, Jéssica Leite Garcia1,
Vânia dos Santos Nunes-Nogueira1, Artur Junio Togneri Ferron1,
Klinsmann Carolo dos Santos1, Fabiane Valentini Francisqueti-Ferron1*
and Camila Renata Corrêa1
1Medical School, São Paulo State University (UNESP), Botucatu, SP, Brazil.
2Institute of Biosciences, São Paulo State University (UNESP), Botucatu, SP, Brazil.
Authors’ contributions
This work was carried out in collaboration among all authors. Authors LCT, FVFF, AJTF and CRC
designed the study. Authors AJTF, DTP and FVFF performed the statistical analysis. Authors LCT,
APCRF, CRC and IOM wrote the protocol and authors LCT, APCRF, FVFF, JLG and CRC wrote the
first draft of the manuscript. Authors KCS, DTP, IOM, VSNN and JLG managed the analyses of the
study. Authors KCS, LCT and FVFF managed the literature searches. All authors read and approved
the final manuscript.
Article Information
DOI: 10.9734/AJARR/2020/v13i230306
(1) Dr. Weimin Gao, Arizona State University, Arizona.
(1) Rabeharitsara Andry Tahina, Polytechnic University of Antananarivo, Madagascar.
(2) Rayenne Djemil, University of Guelma, Algeria.
Complete Peer review History:
Received 07 June 2020
Accepted 14 August 2020
Published 22 August 2020
Aims: To test if the level of oxidative stress is different in women with overweight and with
metabolic syndrome.
Study Design: Cross- sectional.
Place and Duration of Study: Endocrinology Clinic of the Botucatu Medical School- UNESP,
between March 2013 and March 2014.
Methodology: Eighty women (31.15 ± 7.91 years old) attended at the Endocrinology Clinic of the
Botucatu Medical School- UNESP composed this study. According to the body mass index (BMI)
Original Research Article
Talon et al.; AJARR, 13(2): 43-52, 2020; Article no.AJARR.60210
they were divided in 3 groups: Group 1 (G1, n=36 eutrophic); Group 2 (G2, n=21 overweight) and
Group 3 (G3, n=23 women with MS-Metabolic syndrome). It was evaluated: dietary intake of macro
and micronutrients dietary; antioxidant capacity (HAC) of plasma and levels of malondialdehyde
(MDA); carotenoids, retinol and α-tocopherol in peripheral lymphocytes and the comet assay.
Results: Damage to DNA, oxidized purines and the levels of MDA didn’t differ between women
with overweight and with metabolic syndrome but they are higher than those in the control group.
Correlation was positive for BMI and waist circumference (WC) with damage to DNA. Linear
regression showed that higher consumption of protein and sodium is related to damage to DNA
and both carotenoids and omega- 3 are protectors.
Conclusion: Damage to DNA occurs independent of overweight or obesity and WC could be a
predictor for damage to DNA.
Keywords: Body Mass Index (BMI); DNA damage; dietary intake; Metabolic Syndrome (MS).
Obesity is a multifactorial condition leaded
by genetic, behavioral, environmental and
socioeconomic factors. However, nowadays a
sedentary lifestyle and a high caloric intake from
sugar and processed foods are also responsible
by this epidemic condition [1]. Estimative from
World Health Organization demonstrated that in
2016, 39% of adults aged over 18 years were
overweight and 13% were obese [2].
A clinical definition of obesity, useful in many
contexts, is the body mass index (BMI)
30.0 kg/m2 [3]. However, it is clear that BMI is a
poor indicator of body fat rate since it does not
differentiates fat or lean mass [4]. Within context,
waist circumference (WC) has been shown to
predict visceral fat, thus reinforcing the use both
BMI and waist circumference in clinical practice
to evaluate the risk of metabolic disorders [3].
Metabolic syndrome is a condition usually
associated with obesity, and considered a public
health problem in many countries since it
increases the risk for cardiovascular disease
(CVD), type 2 diabetes, hypertension,
dyslipidemia and several cancers [5]. Oxidative
damage, produced by intracellular reactive
oxygen species (ROS), results in modification in
DNA base, breaks in single-strand and double-
strand, and lesions in apurinic/apyrimidinic, many
of them are toxic and/or mutagenic [6].
Therefore, not only ROS are implicated in the
etiology of disease, but the result of DNA
damage may also be a direct contributor to
deleterious biological consequences [7]. A
relationship among increased production of ROS,
impairment of the antioxidant defense,
peroxidative damage to membrane, and
processes inflammatory in degenerative disease
has been demonstrated [8]. Thus, the evaluation
of biomarkers of oxidative stress can help
explore the relation between oxidative damage to
macromolecules (such as DNA, lipids, and
proteins) and several diseases [9].
In according with some researches, human
disorders are proportional to the increase in
adipose mass, specially visceral fat [1012].
Excessive body fat would lead to an increased
formation of ROS resulting in oxidative stress [7],
however the results are inconclusive. So, the aim
of this study was to test if oxidative stress level is
different in women with overweight and with
metabolic syndrome.
2.1 Subjects
Cross- sectional Study performed between
March 2013 and March 2014 at the
Endocrinology Clinic of the Internal Medicine
Department, Botucatu Medical School, São
Paulo State University (UNESP).
The criteria of selection included: non-consumers
more than 60 g/day of alcohol; non-smoking
subjects; non-users of statins; non users of
antioxidant supplements during the sixty days
before this study; no altered hematological
parameters and albumin; no liver and kidney
dysfunction; no cancer, diabetes or altered
thyroid function.
The subjects studied were part of a group
(convenience sample) of participants followed in
the Endocrinology clinic. So, based on inclusion
criteria, 80 women (mean age of 31.15 ± 7.91
years) composed this study. According to their
body mass index (BMI), they were divided into
three groups: Group 1 (G1, the control group):
36 women with a BMI between 18.5 and
Talon et al.; AJARR, 13(2): 43-52, 2020; Article no.AJARR.60210
24.9kg/m2; Group 2 (G2): 21 women with BMI
between 25 to 29.9kg/m2, classified as women
with overweight; and Group 3 (G3): 23 women
with MS [Metabolic Syndrome was specified
according to the International Diabetes
Federation (2005)] [13].
2.2 Anthropometric Analysis
It was measured the body mass of participants
(kg), height (cm), and waist circunference (cm).
Body mass was measured using a portable scale
accurate to 0.1kg (PL 200, Filizola S.A., São
Paulo, Brazil). The height was measured with a
stadiometer accurate to 0.5cm (Professional
Stadiometer Sanny, São Paulo, Brazil). The
waist circumference (WC) was measured at the
narrowest level between the rib margin and the
iliac crest using a non-flexible anthropometric
tape precise to 0.1mm (SN-4010, Sanny, São
Paulo, Brazil). It was also calculated the subjects'
body mass index (BMI = [body weight ÷
(height)2]). All the procedures were done by
health professionals previously trained for the
data collection.
2.3 Blood Pressure (BP)
The BP was measured at rest in the left superior
limb according to recommendation by the
American Heart Association, using a digital BP
monitor (Digital Omron BP Monitor, Model 11
EM403c, Tokyo, Japan). For each measurement,
the subjects rested for 15minutes in the sitting
position with their feet supported and kept their
arm at the heart level.
2.4 Dietary Intake
Habitual food intake was assessed using three
non-consecutive days (two week days and a
week-end day) dietary records. The amounts of
foods registered by trained professional were
converted into grams for the analysis of energy,
macro and micronutrient and dietary fiber intake
using the Diet Pro®software version 5.1i. The
diet records were analyzed by a single person.
2.5 Plasma Analysis
After 12h overnight fasting, it was obtained the
plasma for determination of glucose,
triglycerides, total cholesterol and fractions, urea,
creatinine, ALT (alanine aminotranferase), AST
(aspartate aminotransferase), uric acid and blood
counts by using an automatic enzymatic analyzer
system (Chemistry Analyzer BS-200, Mindray
Medical International Limited, Shenzhen, China).
All the analysis were performed at the Botucatu
Medical School- UNESP.
2.5.1 Extraction of lymphocytes
The level of DNA damage (comet assay) was
evaluated in the peripheral blood lymphocytes.
Blood samples (3ml) were collected into tubes
with 3 ml of RPMI 1640 medium (Sigma-
Aldrich), placed carefully on 3 ml Histopaque ®
1077 (Sigma-Aldrich) and centrifuged at
2500rpm for 30 minutes at 10°C. The
lymphocytes layer was removed and
mixed with 3ml RPMI 1640 medium and
centrifuged again at 1500 rpm for 15 min. After
this procedure, the supernatant was
discarded and lymphocytes were re-suspended
to be used for DNA damage evaluation by comet
2.5.2 Comet assay
The comet assay was an adaptation of the
protocols described by Singh and collaborators
[14] and Tice and collaborators [15]. Clean slides
were briefly dipped into a container with standard
melting point agarose (Sigma-Aldrich] diluted in
1.5% (300 mg/20 mL) PBS buffer (Sigma-
Aldrich) (free of Ca2+ and Mg2+). After this
procedure, the slides was dried at room
temperature. In the next day 10µl of lymphocytes
was added to 120µl of low melting point agarose,
diluted in 0.5% (100mg/20 mL) PBS buffer
(Sigma- Aldrich) (free of Ca2+ and Mg2+). This
suspension was placed on two previously
prepared and identified slides and then
overlaid with covers lips (24 x 60 mm) and
placed at 4°C for 10 minutes to solidify the
After this period, covers lips were removed and
slides were placed in containers, with ice-cold
solution of freshly prepared lysis and (2.5 M
NaCl, 100 mM EDTA, 10mM Tris, Triton X-100
and 1% DMSO), where they remained in the dark
for a period of 24 hours at 4°C. In order to
increase the specificity of the assay, two sheets
per individual were treated with endonuclease III
enzymes (endo III) and formamidopirimidina-
DNA glycosylase (FPG) (BioLabs® Inc,
Ipswich,MA,USA) capable of detecting
pyrimidines and oxidized purines, respectively
[16]. After cell lysis, the slides were placed in a
container containing PBS (Ca2+ and Mg2+ free)
for 5 minutes and then transferred to a flask
containing Flare 1x (40mM Hepes, 0.1M KCl,
Talon et al.; AJARR, 13(2): 43-52, 2020; Article no.AJARR.60210
bovine serum albumin (BSA) buffer 0.2 mg/mL
and 0.5 mM EDTA, pH 8, (sigma-aldrich)) for 5
minutes. This procedure was repeated three
After being placed in a moist chamber, the slides
were treated with 50 mL buffer (950 µL Milli-Q
H2O, 40mL Flare 10x and 10mL BSA, control) or
50mL endo III (1:1000 dilution) or 50mL FPG
(dilution 1: 1000), covered with a cover slip and
incubated for 45 minutes at 37oC. Then the
slides were placed in a refrigerator for 10
minutes to solidify the agarose. After this period,
the covers lips were carefully removed and the
slides transferred to the electrophoresis tank,
filled with cold, freshly prepared alkaline buffer
(1mM EDTA and 300mM NaOH, pH > 13). After
a period of 40 minutes, to unwind DNA,
electrophoresis was performed at 25V and
300mA for 30 minutes. After this step, the plates
were placed for 15 minutes in a neutralization
solution (0.4M Tris, pH 7.5), fixed with 100%
ethanol and allowed to dry at room temperature.
At the moment of analysis, the slides were
stained with 70µL solution of SYBR Gold (2:10
000; Invitrogen, USA), covered with a cover slip
and nucleotides viewed with a fluorescence
microscope (400X magnification) coupled within
image analysis system (Comet Assay II,
Perceptive Instruments, UK). 50 nucleotides per
slide were analyzed. The tail intensity (intensity
of DNA in the tail) was used as a parameter for
assessing levels of DNA damage. The test was
performed in duplicate and analyzed blind with
coded slides.
2.5.3 Plasma Hydrophilic Antioxidant
Capacity (HAC)
The hydrophilic antioxidant capacity in plasma
was determined fluorometrically, as described by
Beretta et al. (2006) [17] using a VICTOR X2
reader (Perkin Elmer, Boston, MA). The
antioxidant activity was quantified by comparing
the area under the curve relating to the oxidation
kinetics of the suspension phosphatidylcholine
(PC), which was used as reference biological
matrix. The peroxyl radical 2’,2’-azobis-(2-
amidinopropane) dihydrochloride (AAPH) was
used as an initiator of the reaction. The results
represent the percent inhibition (4,4 difluoro-5-(4-
phenyl 1-3 butadiene)-4-bora-3,4-diaza-s-
indacene) (BODIPY) 581/591 plasma with
respect to the control sample of BODIPY
581/591 PC liposome. All analyses were
performed in triplicate. The results are reported
as percentage of protection.
2.5.4 Plasma antioxidants levels
Carotenoids, retinol and α-tocopherol were
measured in 100µL of plasma by reversed-phase
high performance liquid chromatography (HPLC;
Waters Alliance 2695 Separation Module,
Waters, Wilmington, MA, USA). The column
used was C30 (Waters Alliance, YMC
carotenoid: 4.6 x 150mm; 3.0μm). The
measurements were performed as previously
described by Yeum and collaborators [18].
2.6 Statistical Analysis
Groups were compared by One-way ANOVA
followed by Tukey's multiple comparison test for
symmetrical data. Non-symmetric data were
analyzed using a generalized linear model with
gamma distribution followed by the Wald
adjusted multiple comparison test. Through
Pearson's correlation coefficient, variables which
were in a significant relationship to the DNA
damage and oxidative damage to purines and
pyrimidines were determined. A stepwise
multiple linear regression model was used to
assess which nutrients influence DNA damage,
considering DNA damage as continuous
response variable and the intake of nutrients as
explanatory variables. Data are presented as
means and standard deviations. All the tests
were performed using SAS for Windows, v9.3.
with a significant level at 5%.
3.1 Results
3.1.1 Anthropometric data and blood
Women with overweight (G2) and with metabolic
syndrome (G3) presented weight, BMI, WC and
SBP higher than the control group, with G3
presenting the highest values. DBP was high
only in G3. There was no difference for height
(Table 1).
3.1.2 Biochemical determinations
Table 2 shows plasma biochemical parameters.
Total cholesterol didn’t differ among groups and
HDL-cholesterol was lower in G3 in comparison
to the other groups. LDL-cholesterol and
triglycerides presented increased levels in G2
and G3 compared to G1. About glucose levels,
G2 and G3 presented higher levels compared to
G1, but the highest levels were found in G3
(Table 2).
Talon et al.; AJARR, 13(2): 43-52, 2020; Article no.AJARR.60210
3.1.3 Macronutrients intake
The dietary intake of macronutrients and
micronutrients are presented in Table 3. Except
for protein (higher in G3) all the others didn’t
present difference among the groups. Regarding
the micronutrients intake, the consumption of
vitamin C and vitamin D was lower in G3
compared to the other groups. All the other
micronutrients didn’t present difference.
3.1.4 Antioxidants in plasma
The concentrations of antioxidants are presented
in Table 4.
Cryptoxanthin and α- carotene were reduced in
G3. On the other hand, uric acid and retinol were
increased in G3. There was no difference among
the groups for lutein, lycopene and α-tocopherol.
3.1.5 Biomarker of oxidative stress and
damage to DNA
Table 5 shows the damage to DNA, total
antioxidant capacity (TAP) and levels of
malondialdehyde (MDA) in each group. About
the damage to DNA, it is important to emphasize
that both G2 and G3 presented more damage
compared to G1. The same pattern was
observed in oxidative damage to purines.
Damage to pyrimidines was higher according to
the nutritional status (G1 < G2 < G3). Total
antioxidant capacity was increased in G3. MDA
levels was higher in G2 and G3 compared to G1.
3.1.6 Correlation among BMI, WC, DNA
damage, oxidative damage to purines
and oxidative damage to pyrimidines
Fig. 1 shows the correlation between DNA
damage and BMI (Fig. 1A) and between DNA
damage and WC (Fig. 1D). Both anthropometric
variables presented correlation with DNA
damage, such as: BMI and oxidative damage to
pyrimidines (Fig. 1B), BMI and oxidative damage
to purines (Fig. 1C), WC and oxidative damage
to pyrimidines (Fig. 1E) and WC and oxidative
damage to purines (Fig. 1F). However, the
correlation between DNA damage and WC was
3.1.7 Association between DNA damage,
consumption of macro and
micronutrients and plasmatic variants
The final linear regression model showed a
positive association between the consumption of
sodium and protein and DNA damage. On the
other hand, polyunsaturated fat intake and
plasma levels of α-carotene were negatively
associated with DNA damage (Table 6).
3.2 Discussion
The aim of this study was to evaluate if the
oxidative stress is different in women with
overweight and with metabolic syndrome. Our
results showed that the damage to DNA already
occurs in women with overweight. Moreover, it
was also demonstrated that increased waist
circumference is associated with DNA damage,
independent of the level of BMI.
Regarding the anthropometric and biochemical
parameters, BMI, waist circumference, diastolic
and systolic blood pressure, and glucose were
higher in group with metabolic syndrome (G3)
compared to overweight group (G2). Several
studies found this same result [1922]. Many
chronic diseases are also result from obesity
(e.g., metabolic syndrome, diabetes mellitus,
liver and cardiovascular diseases, and cancer).
Obesity is associated with low-grade chronic
systemic inflammation in adipose tissue that
promotes pro-inflammatory status exercising a
critical role in the pathogenesis of obesity-related
disorders [23].
Although medical and epidemiological literature
studying the relationship between diet
composition and a variety of illnesses such as
cardiovascular disease, high blood pressure, and
diabetes [24,25], our results show no difference
in the intake for the most of macronutrients and
micronutrients among the groups. Even being a
non expected result, the literature reports some
possible explanation for this: a- the patient
forgets to report the food consumed (omission
errors), as soon reporting foods that have not
been consumed; b- obese people tend to
underestimate their food intake [26].
Reactive oxygen species (ROS) occur under
physiological conditions and in many diseases
causing direct or indirect damage in different
organs; thus, it is known that oxidative stress
(OS) is involved in pathological processes such
as obesity, diabetes, cardiovascular disease, and
atherogenic processes. It has been reported that
obesity may induce systemic OS, a condition
associated with an irregular production of
adipokines, which contributes to the development
of the metabolic syndrome [27]. Interestingly,
damage to DNA, oxidative damage to purines
and the levels of MDA were the same in
Talon et al.; AJARR, 13(2): 43-52, 2020; Article no.AJARR.60210
overweight and metabolic syndrome women and
higher compared to control group even with no
difference in plasma antioxidant levels among
the groups. Studies show that not only an
increase in fat mass leads to an increased
oxidative stress and consequently to oxidative
damage, but also metabolic syndrome and type II
diabetes usually aggravate oxidative stress and
damage [28]. However, different from the
literature our data showed that the damage to
DNA is the same in overweight and MS
Added to this, our results show a correlation
between BMI and WC with damage to DNA,
oxidative damage to purines and pyrimidines.
Considering this, the results suggest that WC
could be used as a predictor for oxidative stress
and DNA damage in conditions which is not
possible to analyze oxidative stress parameters.
Corroborating this, although the current
classification of obesity is based on the Body
Mass Index (BMI), which is the weight (in
kilograms) divided by the square of height (in
meters), BMI has limitations because it does not
distinguish between lean mass and fat; it may
overestimate body fat in well-trained body
builders and underestimate body fat in older
persons. Moreover, BMI does not identify fat
distribution. So, it is now well recognized that
abdominal fat is a major risk for obesity-related
diseases, contributing to pro-oxidant and pro-
inflammatory states, as well as to alterations in
glucose and lipid metabolisms [29].
The final linear regression for damage to DNA
was negative for α- carotene and
polyunsaturated fat acid. The literature shows
that carotenoid can prevent oxidative stress and
DNA damage [30,31] as well as polyunsaturated
fat acid, especially omega-3 from cold water fish
[32]. The literature also reports that n-3
polyunsaturated fatty acids increases the levels
of HDL cholesterol and decrease LDL cholesterol
[33] and protect against autoimmune diseases,
type 2 diabetes, rheumatoid arthritis and cancer
[34]. On the other hand, the final linear
regression for damage to DNA was positive for
protein and sodium. Studies show that diets high
in sodium may predispose individuals not only to
the development of obesity but also to
complications such as hypertension [35,36].
Moreover, sodium intake was also positively
correlated with oxidative stress in experimental
studies; however, the mechanism responsible for
this effect is still being studied, but it has been
suggested that a high-salt diet stimulates the
formation of reactive species through the
activation of NADPH oxidase [37].
Table 1. Anthropometric data and blood pressure in women control (G1), with --overweight
(G2) and with metabolic syndrome (G3)
G1 (n=36)
G2 (n=21)
Age (years)
27.10 ± 4.7 a
33.8 ± 8.5 b
Weight (kg)
55.5 ± 5.0 a
75.2 ± 6.9 b
Height (m)
1.62 ± 0.05 a
1.65 ± 0.07 a
BMI (kg/m2)
21.1 ± 1.7a
27.7 ± 1.8 b
WC (cm)
70.4 ± 5.5 a
89.2 ± 6.6 b
SBP (mmHg)
109 ± 9 a
116 ± 10 b
DBP (mmHg)
71.7 ± 7.7 a
76.2 ± 6.5 a
BMI = body mass index, WC = waist circumference, SBP = systolic blood pressure, DBP = diastolic blood pressure.
Results are expressed as means and standard deviation. Means followed by different superscript letter indicating
whether significant differences among groups (ANOVA followed by Tukey’s test at p < 0.05)
Table 2. Plasma biochemical profile in control (G1), overweight (G2) and metabolic syndrome
(G3) women
G1 (n=36)
G2 (n=21)
G3 (n=23)
Cholesterol (mg/dL)
184 ± 31 a
204 ± 31 a
198 ± 25 a
HDL-cholesterol (mg/dL)
68.1 ± 16.9 a
61.4 ± 15.0 a
46.0 ± 10.7 b
LDL-cholesterol (mg/dL)
98.6 ± 31.8 a
117 ± 36ab
122 ± 26 b
88.4 ± 31.1 a
122 ± 63 b
149 ± 60b
Glucose (mg/dL)
73.2 ± 4.7 a
78.9 ± 6.8 b
85.5 ± 7.7 c
Results are expressed as means with standard deviation. Means followed by different superscript letter indicating
whether significant differences among groups (ANOVA followed by Tukey’s test at p < 0.05)
Talon et al.; AJARR, 13(2): 43-52, 2020; Article no.AJARR.60210
Table 3. Dietary intake of macronutrients and micronutrients in control (G1), overweight (G2)
and metabolic syndrome (G3) women
G1 (n=36)
G2 (n=21)
G3 (n=23)
Carbohydrate (g)
207 ± 76 a
215 ± 81 a
208 ± 64 a
Cholesterol (mg)
176 ± 90 a
184 ± 76 a
195 ± 117 a
Fiber (g)
14.1 ± 6.7 a
12.2 ± 5.0 a
11.8 ± 3.8 a
Monounsaturated fat (g)
13.4 ± 6.6 a
14.3 ± 7.1 a
14.1 ± 6.5 a
Polyunsaturated fat (g)
9.9 ± 5.2 a
9.9 ± 9.0 a
8.9 ± 4.0 a
Saturated fat (g)
13.1 ± 7.2 a
14.3 ± 6.3 a
12.7 ± 6.0 a
Total fat (g)
59.4 ± 19.4 a
65.6 ± 30.7 a
57.0 ± 20.9 a
Protein (g)
70.7 ± 20.3 a
75.3 ± 20.9 ab
105 ± 133 b
Calcium (mg)*
637 ± 199 ab
586 ± 348 a
442 ± 284 b
Iron (mg)**
37.9 ± 99.2 a
36.4 ± 112.1 b
11.0 ± 4.6 a
Folate (µg)**
152 ± 74 a
149 ± 65 a
134 ± 38 a
Phosphorus (mg) *
802 ± 244 a
803 ± 254 a
772 ± 173 a
Magnesium (mg)*
159 ± 79 a
213 ± 199 a
135 ± 35 a
Potassium (mg) *
1764 ± 635 a
2037 ± 1650 a
1565 ± 438 a
Selenium (µg) **
79.6 ± 82.7 a
81.2 ± 79.6 a
70.2 ± 29.2 a
Sodium (mg) **
1705 ± 667 a
2447 ± 1322 b
2130 ± 730 ab
Vitamin A (equiv. retinol)**
794 ± 401 a
649 ± 434 a
631 ± 486 a
Vitamin C (mg)**
148 ± 131 a
78.8 ± 47.1 b
79.8 ± 53.0 b
Vitamin D (µg)**
25.6 ± 49.9 a
3.62 ± 8.24 a
3.18 ± 5.55 b
Vitamin E (mg)**
76.3 ± 243.9 ab
41.6 ± 139.9 a
12.7 ± 6.3 b
Zinc (mg)**
10.2 ± 22.4 a
16.4 ± 34.3 a
17.3 ± 30.0 a
Results are expressed as means with standard deviation. Means followed by different superscript letter indicating
whether significant differences among groups (ANOVA followed by Tukey’s test at p < 0.05). * ANOVA followed by
Tukey’s multiple comparison test. ** Generalized linear model with gamma distribution followed b y Wald multiple
comparison test
Table 4. Plasma carotenoids, α-tocopherol, uric acid and retinol of women control (G1), with
overweight (G2) and with metabolic syndrome (G3)
G1 (n=36)
G2 (n=21)
G3 (n=23)
Lutein (µg/dL)
8.35 ± 6.13 a
5.13 ± 3.10 a
7.72 ± 6.54 a
Cryptoxanthin (µg/dL)
18.9 ± 18.4 a
10.1 ± 9.2 ab
7.86 ± 8.45 b
α-carotene (µg/dL)
5.75 ± 4.57 b
2.63 ± 1.49 a
2.76 ± 1.69 a
β-carotene (µg/dL)
12.2 ± 11.5 a
6.32 ± 3.99 ab
5.22 ± 3.36 b
Lycopene (µg/dL)
5.87 ± 6.94 a
6.09 ± 5.26 a
6.06 ± 5.86 a
α-tocopherol (µg/dL)
491 ± 254 a
462 ± 242 a
626 ± 255 a
Uric acid (mg/dL)
3.75 ± 0.77 a
4.39 ± 1.09 b
5.32 ± 1.14 c
Retinol (µg/dL)
80.2 ± 34.6 ab
68.4 ± 29.6 a
106 ± 77 b
Results are expressed as means and standard deviations Means followed by different superscript letter indicating
whether significant differences among groups (generalized linear model with gamma distribution followed by Wald
multiple comparison test at 5%)
Table 5. DNA damage, total antioxidant capacity (TAP), malondialdehyde (MDA) levels in
women control (G1), with overweight (G2) and with metabolic syndrome (G3).
G1 (n=36)
G2 (n=21)
G3 (n=23)
DNA damage (%) **
49.9 ± 9.0a
76.7 ± 13.3b
76.1 ± 9.9b
Oxidative damage to purines (%)**
60.8 ± 10.3 a
81.4 ± 11.3 b
76.7 ± 9.9 b
Oxidative damage to pyrimidines (%)**
54.2 ± 10.6 a
84.8 ± 4.6 b
71.7 ± 10.7 c
TAP (%) *
37.8 ± 12.4 a
44.0 ± 14.4 ab
51.3 ± 10.1 b
MDA (umol/L)*
12.6 ± 8.4 a
34.5 ± 18.0 b
41.2 ± 20.0b
Results are expressed as mean and standard deviation Means followed by different superscript letter indicating whether
significant differences among groups. ** Generalized linear model with gamma distribution followed by Wald multiple
comparison tests. * ANOVA followed by Tukey's multiple comparison tests (p < 0.05). TAP= total antioxidant capacity,
MDA = malondialdehyde
Talon et al.; AJARR, 13(2): 43-52, 2020; Article no.AJARR.60210
Table 6. Final linear regression model relating DNA damage with consumption of macro and
micronutrients and plasmatic variants
P value
< 0.0001
α-carotene (µg/dL)
Polyunsaturated fat (g)
Protein (g)
Sodium (mg)
< 0.0001
Fig. 1. Correlation between BMI and DNA damage (A); BMI and oxidative damage to
pyrimidines (B), BMI and oxidative damage to purines (C), WC and DNA damage (D), WC and
oxidative damage to pyrimidines (E), WC and oxidative damage to purines (F). BMI- body mass
index (kg/m²); WC- waist circumference (cm). Pearson Correlation between the variables
In summary, this paper brings important finds:
increased BMI is associated with metabolic
syndrome, higher BMI and waist circumference is
associated with damage to DNA and oxidative
stress but damage to DNA is the same in
overweight and MS women, and high intake of
protein and sodium increases damage
to DNA. So, it is possible to conclude that
increased BMI and waist circumference is
related to increased damage to DNA but is not
different between overweight and metabolic
syndrome women. It is also suggested
that WC could be used as predictor of damage to
The Ethics Committee on Human Research
from the same university approved the study
protocol (Protocol 3788-2011) and the written
informed consent was obtained from all
The authors gratefully acknowledge:
Processo n.2011/08373-5, Fundação de
Amparo à Pesquisa do Estado de São Paulo
(FAPESP) for financial support.
Authors have declared that no competing
interests exist.
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... In addition to fueling the growth of breast cancer, obesity has also been hypothesized to drive breast cancer initiation (Figure 1). A growing number of studies have highlighted an apparent genomic instability associated with obesity (91)(92)(93)(94). This is significant since genomic instability can lead to mutations that lead to tumorigenesis (95). ...
... For example, in one study DNA damage in peripheral blood lymphocytes was measured utilizing the comet assay that quantitates breaks in DNA. Both BMI and waist circumference were positively associated with DNA damage (94). Similar findings were made in an aging study, where obesity was a stronger predictor of skeletal muscle DNA damage compared to aging (96). ...
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Obesity is gaining acceptance as a serious primary health burden that impairs the quality of life because of its associated complications, including diabetes, cardiovascular diseases, cancer, asthma, sleep disorders, hepatic dysfunction, renal dysfunction, and infertility. It is a complex metabolic disorder with a multifactorial origin. Growing evidence suggests that oxidative stress plays a role as the critical factor linking obesity with its associated complications. Obesity per se can induce systemic oxidative stress through various biochemical mechanisms, such as superoxide generation from NADPH oxidases, oxidative phosphorylation, glyceraldehyde auto-oxidation, protein kinase C activation, and polyol and hexosamine pathways. Other factors that also contribute to oxidative stress in obesity include hyperleptinemia, low antioxidant defense, chronic inflammation, and postprandial reactive oxygen species generation. In addition, recent studies suggest that adipose tissue plays a critical role in regulating the pathophysiological mechanisms of obesity and its related co-morbidities. To establish an adequate platform for the prevention of obesity and its associated health risks, understanding the factors that contribute to the cause of obesity is necessary. The most current list of obesity determinants includes genetic factors, dietary intake, physical activity, environmental and socioeconomic factors, eating disorders, and societal influences. On the basis of the currently identified predominant determinants of obesity, a broad range of strategies have been recommended to reduce the prevalence of obesity, such as regular physical activity, ad libitum food intake limiting to certain micronutrients, increased dietary intake of fruits and vegetables, and meal replacements. This review aims to highlight recent findings regarding the role of oxidative stress in the pathogenesis of obesity and its associated risk factors, the role of dysfunctional adipose tissue in development of these risk factors, and potential strategies to regulate body weight loss/gain for better health benefits.