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2017; 63(1):85-91

fied by comparing the area under the curve (AUC) on the

oxidation kinetics of BODIPY (4,4-difluoro-1,3,5,7,8-

pentamethyl-4-bora-3a, 4a-diaza-s-indacene), a fluorescent

lipophilic oxidizable compound, radical initiator opposite

2.20 azobis- (2-amidinopropane) dihydrochloride (AAPH)

in relation to the oxidation of phosphatidylcholine used

as a reference lipid matrix.

Another approach to assess the antioxidant capacity

is to measure antioxidants individually. However, as there

are many, this would require time and a variety of ana-

lytical techniques, instruments, and procedures. In addi-

tion, this approach lacks information about the possible

synergy and cooperation between the hydrophilic and

lipophilic antioxidants.

Protein and DNA molecules are also highly suscep-

tible to modification by changes in redox state.

The

protein oxidation occurs when proteins of amino acids

(proline, arginine, threonine, lysine, histidine and cysteine)

bind to glycoxidation and lipoxidation products, forming

carbonyl groups. This reaction called carbonylation may

be irreversible and lead to changes in their biological

function; the detection of these toxic products (carbonyl)

can be made by the mass spectrometer.

As for DNA damage, comet assay can be performed,

a cell microgel electrophoresis technique, very useful and

widely used to assess damage and DNA repair in indi-

vidual cells. Its basic principle is the lysis of cell membranes,

followed by induction of DNA released from the electro-

phoretic migration on agarose matrix. When viewed un-

der a microscope, the migrated cell takes the apparent

form of a comet, with a head, the nuclear region, and a

tail, which contains fragments or DNA strands that have

migrated towards the anode. The analysis of comets is

based on the degree of DNA fragmentation and migration

by microelectrophoresis.

Measures such as the total

length of the “tail” and the DNA density provide indirect

information about the state of the sample DNA. To detect

oxidative damage, endonuclease III (ENDOIII) and phos-

phatidylinositol-pyrimidine DNA glycosylase (FPG) are

used to repair enzyme thus detecting oxidation bases in

the pyrimidine and purine.

ietary

intake

physical

activity

oxidative

stress

and metabolic

syndrome

According to what has been previously described, it is

clear that when there is an imbalance within a large sup-

ply of nutrients and a low antioxidant intake, obesity

carries a picture of oxidative stress promoting metabolic

syndrome.

Corroborating this fact, the literature indi-

cates that individuals with metabolic syndrome and obe-

sity have a high consumption of fat and sugars derived

from processed foods with high sodium content,

49-51

well as low antioxidant intake.

Diets with high antioxidant content, such as the well-

-known Mediterranean diet, which consists of olive oil,

fruits and vegetables, cereals, nuts, and a small amount

of red meat and foods high in sugar, are also ways to

manage oxidative stress and inflammation.

52,53

Research-

ers suggest that individuals with MetS and obesity delayed

and attenuated complications, such as insulin resistance,

hypertension, and hyperlipidemia, when they had an

intervention and began to consume this type of diet. One

of the arrangements set out for this improvement was

the reduction of oxidative stress and inflammation.

53-57

Among these studies, Mitjavila et al.

observed a de-

crease of some markers of oxidative stress after one year

of dietary intervention. In this same study, subjects with

MetS who consumed the Mediterranean diet were com-

pared to a group that consumed a diet with only low

levels of fat. It showed that a diet richer in antioxidants

resulted in improvement in markers of oxidative stress

and decreased DNA damage. This shows the importance

of diet quality and the consistency and effectiveness of

antioxidants in its composition.

Another factor associated to MetS is reduced daily

physical activity in healthy young adults, which leads to

negative metabolic consequences such as decreased insu-

lin sensitivity and increased abdominal fat.

Therefore,

increased physical activity is likely to be the evolutionary

favored pathway to prevent the development of insulin

resistance during metabolic derangements. The impact

of exercise on insulin sensitivity is evident for 24 to 48

hours and disappears within 3 to 5 days, so continuous

practice is essential.

Besides, exercise increases the pro-

duction of oxidative stress. However, these increases seem

to be necessary in order to allow for an upregulation in

endogenous antioxidant defenses, thus providing benefi-

cial effects to the individual engaged in chronic exercise.

A combination of resistance and aerobic exercise is the

best, but any activity is better than none.

The association between good eating habits and exer-

cise practice is also important. A recent study showed that

food adequacy (intake of fruits and vegetables) associated

with physical exercise for 20 weeks resulted in higher car-

diorespiratory fitness in residents of the city of Botucatu,

SP. Moreover, reduction in visceral adiposity (waist circum-

ference) was observed, reducing the prevalence of MetS

and mainly increasing significantly glutathione concentra-

tion and total antioxidant protection (TAP) of the plasma.

Dietary caloric restriction as well as aerobic exercise, an-