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International Journal of Medical Research &
Health Sciences, 2019,
148
ISSN No: 2319-5886
ABSTRACT
Background: Liver is the most important organ performing more than 500 functions in the body. In addition, the
human cell has a natural antioxidants system which maintains the production of antioxidants and reactive oxygen
species (ROS) during the metabolic process of the cell. Objective: This particular research study is basically conducted
for the purpose to assess the impact of low-intensity exercise on liver enzymes and antioxidants systems of the body.
Methods and materials: Total 40 subjects (20 from low-intensity exercise as an experimental group and 20 subjects
as a control group) were included as the participants of the study. For assessment of liver functions and redox state of
the body, 5 ml blood was collected from all subjects. Liver functions tests (LFTs) were performed for the assessment of
liver enzymes and ferric reducing assay protocols (FRAP) was performed for the assessment of the redox state of the
body. The data obtained about liver functions and redox state were processed through statistical package for social
sciences (SPSS) version 23 and thus different statistical tools i.e. mean, standard deviation and T-score were used for
the analysis of data. Results: Data analysis reveals that; no signicant effect was found on liver enzymes as well as
on antioxidants system of the body. Conclusion: On the basis of ndings the researcher concluded that low-intensity
exercise has no signicant effects on liver enzymes. In addition, it was also concluded that low-intensity exercise helps
in the improvement of blood life quality by reducing various health problems related to oxidative damages of cells
and muscles fatigue.
Keywords: Low-intensity exercise, Liver, Enzymes, Antioxidants, ROS, FRAP
Impact of Low-Intensity Exercise on Liver Enzymes and
Antioxidants Systems of the Body
Alamgir Khan1*, Salahuddin Khan1, Samiullah Khan2, Shireen Bhatti3 and Shahzaman
Khan4
1 Department of Sports Sciences and Physical Education, Gomal University, Pakhtunkhwa,
Pakistan
2 Gomal Center of Biochemistry and Biotechnology, Gomal University, Pakhtunkhwa, Pakistan
3 Department of Sports Sciences and Physical Education Sukkur IBA University, Sukkur, Sindh,
Pakistan
4 Department of Sports Sciences and Physical Education, University of Lahore, Punjab, Pakistan
*Corresponding e-mail: alamgir1989@hotmail.com
INTRODUCTION
During the process of metabolism free radicals, reactive oxygen and nitrogen varieties are produced by the cells.
As a natural process, the antioxidants system comprised of catalase, superoxide dismutase, glutathione peroxidase,
and many non-enzymatic antioxidants, consisting of vitamins A, E and C, glutathione, ubiquinone, and avonoids
that take away the free radicals [1]. The author further stated that aerobic exercise as the chief offender of enhanced
oxidative stress.
In the biological arrangement of the body, cells respond to moderate oxidative stress by producing their antioxidant
impedance and other protective methods [2]. The capabilities of antioxidants in tissues are well unied to suit the rates
of oxygen intake and radical formation. Oxidation occurs in numerous ways, for instance, in the formation of energy
by the cells using glucose, in the process of immunization when bacteria is to be diminished and to make inammation
and to detoxify harmful waste, pesticides, and cigarette smoke. To add more, oxidation also makes a person free from
physical and/or emotional stress [3].
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-150
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The process of cellular respiration renders us reactive oxygen species (ROS). The ROS regulates gesturing and
homeostasis. During unstable reactive oxygen species and antioxidants, aerobic stress is formed. The physical
exercises also affect the antioxidants and reactive oxygen species (ROS) and result in oxidative stress [3]. Exercises
lead to oxygen consumption and the hectic process eat cells which have been demonstrated by the augmentation of
sarcolemma disruption [4].
Yet this attitude of exercise does not stand for the entire situation. However, it is true that excessive exercise lowers
oxidative stress and consequently, cellular proteins, lipids, and nucleic acids are transformed into the glutathione
system [5]. Exercise also affects the pro and anti-inammatory cytokine formation [6]. Protein which is a basic
component of the cell can be affected due to the overuse or during the continuous performance of exercise and
similarly when proteins level in the cell is affected then it can cause oxidative stress [7].
Free Radicals
The metabolic system ensures the production of free radicals [8]. Free radicals are a molecule or parts of molecules
that have one or more odd number of electrons in the outer cloud layer”. They are thought to be having a very short
half-life and its own specic advanced level of reactivity. Destructive private property of free radicals is due to
their naive inclination to achieve electronic stability. In this way, while nding an opportunity to react with its rst
neighboring stable molecule picking an electron and emerges a new free radical. The affected molecules become
unbalanced itself and enter into reaction with other molecules it gets near to, which caused a disturbance in the
components of cells. Free radicals are generated during the process of oxidative phosphorylation in mitochondria [9].
Free radicals may result in the destruction of cells and their elements. The body does possess a large number of
antioxidant resistivity both for internal and external purposes. These internal and external performance immune the
cellular process from free radical persuaded harm [10]. Following is a categorized process of free radicals.
• Antioxidant enzymes
• Chain breaking antioxidants
• Transition metal binding proteins
Reactive Oxygen and Nitrogen Species (RONS)
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are the 2 coinages used for free radicals and
non-free radicals’ concluded from oxygen and nitrogen. These species can be created by the release or gain of a single
electron. Moreover, superoxide (O2
-•) and nitric oxide (NO•) are the 2 principal oxygen and nitrogen derived free
radical species charged within reactive oxygen and nitrogen species (RONS) [11]. The system of electron transport
chain is one of the principal industry of superoxide (O2-•) in the process of cellular respiration through oxidation.
A large number of free radicals resulting into in vitro or originate from reactive oxygen species (superoxide (O2-•),
hydroxyl (OH•), alkoxyl (RO•), peroxyl (ROO•) and hydroperoxyl (ROOH•) or reac tive nitrogen species (nitric oxide,
nitrogen dioxide, peroxynitrite oxidized) [12].
Physical Activity and Oxidative Stress
Consistent bodily exercise reinforces the immune system and makes one capable of avoiding cardiovascular diseases.
To promote health and avoiding cardiovascular diseases, 30 minutes per day of moderate-intensity physical activity,
including brisk walking are suggested [13]. Bodily exercises have helpful properties such as keeping the level of
cholesterol, healthy muscles, bones and joints and its aids in regulating the body weight [14].
However, active bodily exercise does not incite the same result as long term exercise training. Regular physical
exercise helps the body to get an adjustment and to escape from the harmful effects of oxidative stress [15]. Energetic
or acute bodily exercise can cause oxidative stress and resulting injury to cellular proteins, lipids, and nucleic acids
as well as changes to the glutathione system. It is also obvious that regular exercise permits the antioxidant scheme to
control the making of reactive oxygen and nitrogen species [16].
Research indication shows that severe aerobic physical exercise or training causes oxidative stress chiey when its
intensity and length is more than the approach of the body [17]. Severe muscular exercise results in an augmented
production of free radicals and other forms of reactive oxygen species such as superoxide and hydrogen peroxide.
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The antioxidant system is used to defend the organism from the injurious effects of free radicals. This system contains
antioxidant enzymes (catalase, glutathione peroxidase, superoxide dismutase) and non-enzymatic antioxidants
(vitamin E, vitamin A, vitamin C, glutathione and uric acid). The no uniformity between free radical production and
antioxidant resistance leads to an oxidative stress state.
The high amount of exercise results in an increased amount of reactive and nitrogen species and in this way, the
amount of ROS increases and RNS may cause imbalance among RONS and antioxidants. The resulting oxidative
injury due to oxidation of lipids, proteins, and DNA, is that the bodily exercise no longer helps the body but costs it,
increasing the body vulnerability to exhaustion and often to injury and disease [18].
Bodily exercise may become a source of unstable reactive oxygen species and antioxidants in the body and thus,
this disorder is considered very dangerous due to its negative effect on overall practical abilities of the body [19]. To
achieve success in sports or to carry the sports activities in successful manners one would need to be free from all
kind of psychological as well as physiological stressors. Because any kind of stress either they are physiological or
psychological adversely inuence body performance. High-intensity exercise induces oxidative stress which affects
the performance of a person. Oxidative stress accurses, when free radicals attack the cells similarly it affects the
performance such as; accelerated gaining, muscles pain, anti-inammatory medications and overuse injuries [19].
An imbalance may be created by frequent preformation of exercise in reactive oxygen species and antioxidants thus
may result in oxidative stress [20]. This intern results in various chronic diseases [21]. Muscular exhaustion is very
closely related to oxidative stress [22]. The author further specied that oxidative stress may cause muscles injury
and dysfunction of the immune system. Muscular exercise tempted oxidative stress by generating the reactive species
(ROS) and nitrogen species (RONS) due to metabolic and mechanical stresses during skeletal muscle contractions [23].
Exercise causes oxidative stress. Numerous research studies related to aerobic exercises such as running and cycling
found that aerobic activities need more oxygen consumption (VO2) which culminates in an increase in both free
radical production and activity. However, this phenomenon is not evident at exercising of low intensity (<50% VO2
max) likewise in such case the antioxidant capacity is not exceeded and damages induced by free radicals did not take
place. The making of free radicals and oxidative stress is advanced if a more rigorous physical activity is performed [20].
The principal cause of the production of radicals and other reactive oxygen species (ROS) is muscular exercise.
Research indication shows that an intensied exercise leads the body towards protein oxidation which causes
muscles fatigue. Muscles cells comprise of a complex endogenous cellular resistance (enzymatic and non-enzymatic
antioxidants) to eliminate reactive oxygen species and to decrease the muscles injuries [24]. Muscular exercise ignites
the oxidative stress and so the muscles remain unable to perform the activity because of fatigue. To lessen fatigue and
do the exercise, the body needs to utilize antioxidants supplementations [24].
Exercise is supposed to be the leading cause of bringing increment in the formation of reactive oxygen species
(ROS) possibly causing mutations, tissue, and immune system damage. A stress protein shows one of the common
protective mechanisms which enable the cells and the organism to overcome stress [25,26]. The author further added
that relationship in stress protein, reactive oxygen species (ROS) and physical activity is still needed to be discovered.
MATERIALS AND METHODS
The below procedures were adopted by the researcher for reaching certain ndings and conclusion.
Chemical and Reagents
Analytical grade chemicals such as ferric chloride, 2, 4, 6-tripyridyl- s-triazine (tptz), standard antioxidant “trolox”
(Merck, Germany) dimethylsulfoxide (DMSO), methanol, L-ascorbic acid (Sigma Aldrich, Germany) were used for
the experimental setup of the study.
Participants of the Study
According to Dayan, et al., and Clark, et al., low-intensity exercise is that which gets you to about 40-50% of your
Maximum heart rate (MHR). It includes routine jogging and walking. Based on this justication low intensity exercise
performers were recruited from Department of Sports Sciences and Physical education, Gomal University, Kp,
Pakistan by the application of international physical activity questionnaire (IPAQ).
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Sample and Sample Size
Total 2 different groups of subjects were voluntarily included in the study. One group comprised of 20 subjects of
low-intensity exercise performers (EXG) who were recruited from the Department of Sports Science and Physical
Education Gomal University and thus the second group comprised of 20 subjects, performing no activities (CONT)
was recruited from various departments of Gomal University, KP, Pakistan. Study objectives were explained to the
participants and those who consented and fulll the inclusion criteria were included in the study. During the selection
process of the subjects all those subjects were included in the study that represents the exercise-trained cohort, and
age and sex-matched sedentary control.
Exclusion Criteria
Subjects were excluded from the study by adopting the following exclusion criteria:
• Subject with complete sedation
• Subject taking any kind of medication for long term
• A subject having a chronic disease
• The subject refused written consent of participation
• Subject aged more than 30 years
Blood Sample Collection
Blood samples (5 ml) were collected from all subjects by vein puncture and immediately transferred in heparinized
tubes and centrifuged to separate plasma for determination of ALT, AST, and ALP. Each tube was marked with a
subject distinguishing proof code. For the assessment of redox body state (antioxidants system), serum was excreted
from each blood sample.
Procedures for Excretion of Serum from the Blood
• The collected blood was kept in a freezer at 200°C
• The blood samples were centrifuged at 15000 rpm for 20 minutes at room temperature
• Serum or plasma was separated from the whole blood within 6 hours after sampling
• The serum or plasma was then transferred to sterile polypropylene tubes
Ethical Approval of the Study Protocols
Regarding the protocols of this research study, ethical approval was sought out from the ethical and research board
of Gomal University. Permission was taken from the Department of Sports Sciences and Physical Education, Gomal
University. Written informed consent was taken from the respondents before participating in the process of this
research project. Privacy of participants was safeguarded at all times. Withdrawal policy was also ensured during the
lling of the consent form.
Ferric Reducing Antioxidant Power (FRAP) Assay for the Measurement of Oxidative Stress through Blood
Sample
The antioxidant capacity of the sample was estimated spectrophotometrically following the procedure of Benzie and
Strain. The method is based on the reduction of Fe3+ TPTZ complex (colorless complex) to Fe2+-tripyridyltriazine (blue
colored complex) formed by the action of electron donating antioxidants at low pH. This reaction is monitored by
measuring the change in absorbance at 593 nm. The ferric reducing antioxidant power (FRAP) reagent was prepared
by mixing 200 ml acetate buffer, 20 ml of 10 mM TPTZ, 20 ml of 20 mM ferric chloride (at 10:1:1). The concentration
of ferric tripyridyltriazine (Fe-TPTZ) compound decreases and was converted to the ferrous form at acidic pH.
Statistical Analysis
The data obtained about liver functions and redox state were processed through statistical package for social sciences
(SPSS) version 23 and thus different statistical tools i.e. mean, standard deviation and T-score for the analysis of data.
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RESULTS
There was a comparison of Control group N=20 (CG), Low-intensity exercise group, N-20 (EXG) regarding Body
mass index (BMI), Alanine transferase (ALT), Alkaline phosphate (ALP), Aspartate (AST) and FRAP. Similarly, the
data are articulated as mean, and standard deviation, T- score, and p-value. The data of both groups about; BMI shows
that the mean of CG was 20.95 ± 1.79, mean of EXG was 22.35 ± 1.46, T-value of both CG and EXG was 2.709,
the p-value was 0.010. Therefore signicance difference is found in BMI of both groups CG and EXG (t 38=-2.709,
p<0.05). The BMI of CG was less than the BMI of EXG. ALT shows that the mean of CG was 33.50 ± 2.11, mean
of EXG was 40.60 ± 11.65, T-value of both CG and EXG was -2.680, the p-value was .011. (t 38=-2.680, p<0.05)
Therefore signicance difference was found in ALT of both groups CG and EXG. The ALT of CG was less than
the ALT of EXG. ALP shows that the mean of CG was 40.60 ± 51.54, mean of EXG was 236.90 ± 50.96, T-value
of both CG and EXG was 1.44, the p-value was 0.158 (t 38=1.44, p>0.05). Therefore no signicant difference was
found in ALP of both CG-I and EXG. The ALP of CG was high than the ALP of EXG. AST shows that mean of CG
was 25.35 ± 4.81, mean of EXG was 27.60 ± 5.35, T-value of both CG and EXG was -1.40, the p-value was 0.170 (t
38=1.40, p>0.05). Therefore no signicant difference was found in AST of both Groups CG and EXG. The AST of
CG was less than the AST of EXG. FRAP shows that mean of CG was 138.59 ± 21.83, mean of EXG was 120.90 ±
13.45, T-value of both CG and EXG was 3.08, and the p-value was 0.004 (t 38=3.08, p<0.05). Therefore signicance
difference was found in FRAP value of both groups CG and EXG. The FRAP value of CG was high than the FRAP
value of EXG (Table 1).
Table 1 Mean difference between the BMI, ALT, ALP, AST, and FRAP of Control group (CG) and low-intensity exercise
group (EXG)
Testing Variables Category N Mean SD T Sig.
Body Mass Index Control group 20 20.95 1.79106 -2.709 0.010
LIE 20 22.35 1.46089
Alanine Transferase (IU/L) Control group 20 33.5 2.11511 -2.680 0.011
LIE 20 40.6 11.6592
Alkaline Phosphate (IU/L) Control group 20 236.9 51.54548 1.441 0.158
LIE 20 213.55 50.96074
Aspartate (mg/dl) Control group 20 25.35 4.81527 -1.400 0.170
LIE 20 27.6 5.33509
Ferric Reducing Antioxidant
Power Assay (µmole/L)
Control group 20 138.5925 21.83079 3.085 0.004
LIE 20 120.901 13.45593
Comparison of the low-intensity exercise group, N-20 (EXG) with nutritional supplementation (EXG-A) N-10 and
non-nutritional supplementation (EXG-B) N-10 regarding Body mass index (BMI), Alanine transferase (ALT),
Alkaline phosphate (ALP), Aspartate (AST) and FRAP. Similarly, the data are articulated as mean, and standard
deviation, T-score and p-value. The data about BMI shows that mean of EXG-A was 22.40 ± 1.26, mean of EXG-B
was 22.30 ± 1.70, T-value of both EXG (A and B) was 0.149, the p-value was 0.883 (t18=0.149, p>0.05). Therefore
no signicant difference was found in BMI of both EXG (A) and EXG (B). The BMI of EXG (A) was high than the
BMI of EXG (B). ALT shows that mean of EXG (A) was 30.70 ± 1.33, mean of EXG (B) was 50.50 ± 8.20, T-value
of both EXG (A and B) was -7.528, the p-value was 0.000 (t18=-7.528, p<0.05). Therefore signicant difference was
found in ALT of both EXG (A) and EXG (B). The ALT of EXG (A) was less than the ALT of EXG (B). ALP shows
that mean of EXG (A) was 246.10 ± 33.60, mean of EXG (B) was 181.0 ± 44.7, T-value of both EXG (A and B) was
3.68, the p-value was 0.002 (t18=3.68, p<0.05). Therefore signicant difference was found in ALP of both EXG (A)
and EXG (B). The ALP of EXG (A) was high than the ALP of EXG (B). AST shows that mean of EXG (A) was
29.30 ± 2.40, mean of EXG (B) was 25.90 ± 6.90, T-value of both EXG (A and B) was 1.46, the p-value was 0.159
(t18= 1.46, p>0.05). Therefore no signicant difference was found in AST of both EXG (A) and EXG (B). The AST
of EXG (A) was high than the AST of EXG (B). FRAP shows that mean of EXG (A) was 115.25 ± 12.08, mean of
EXG (B) was 126.55 ± 12.86, T-value of both EXG (A and B) was 2.02, the p-value was 0.058 (t18=2.02, p>0.05).
Therefore no signicant difference was found in FRAP of both EXG (A) and EXG (B). The FRAP of EXG (A) was
less than the FRAP of EXG (B) (Table 2).
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Table 2 Mean difference in BMI, ALT, ALP, AST, and FRAP of low-intensity exercise group (EXG) with nutritional
supplementation (EXG-A) and non-nutritional supplementation (EXG-B)
Testing Variable Supplement N Mean SD t Sig.
Body Mass Index Use Supplement (LIE) 10 22.400 1.26491 0.149 0.883
No Use Supplement (LIE) 10 22.300 1.70294
Alanine Transferase (IU/L) Use Supplement (LIE) 10 30.700 1.33749 -7.528 0.000
No Use Supplement (LIE) 10 50.500 8.20907
Alkaline Phosphate (IU/L) Use Supplement (LIE) 10 246.100 33.60704 3.681 0.002
No Use Supplement (LIE) 10 181.000 44.70645
Aspartate (IU/L) Use Supplement (LIE) 10 29.300 2.40601 1.468 0.159
No Use Supplement (LIE) 10 25.900 6.91938
Ferric Reducing Antioxidant
Power Assay (µmole/L)
Use Supplement (LIE) 10 115.252 12.08049 2.025 0.058
No Use Supplement (LIE) 10 126.550 12.86041
DISCUSSION
The nding of the present study reveals that mean and standard deviation (ALT) of CG was 33.50 ± 2.11, mean of
EXG was 40.60 ± 11.65, T-value of both CG and EXG was -2.680, the p-value was 0.011 (t38=-2.680, p<0.05).
Therefore a signicant difference was found in ALT of both Groups CG and EXG. The ALT of CG was less than
the ALT of EXG. The ndings of studies conducted by George, et al., and Eckard, et al., testied that ALT was
changed among the subjects as a result of low-intensity exercise. They further calculated the statistical difference
in both the control group and the experimental group before and after exercise (SMD -0.40, 95% CI -0.75 ~-0.05,
p=0.03). Findings of the study conducted by Eckard, et al., revealed that with or without nutritional supplementations
(20 intervention groups) the level of ALT was not signicantly altered in 10 groups and was signicantly reduced
(improved) in 5 groups and increased in 5 groups [27].
The study found out that mean and standard deviation (ALP) of CG was 40.60 ± 51.54, mean of EXG was 236.90 ±
50.96, T-value of both CG and EXG was 1.44, the p-value was 0.158 (t38=1.44, p>0.05). Therefore no signicant
difference was found in ALP of both CG-I and EXG. The ALP of CG was higher than the ALP of EXG. This
emerging concept is supported by Statland, et al., and reported that ALP was almost unaltered during the 7-day period
of exercise. Pettersson, et al., concluded that AST and ALT were pointedly increased for at least 7 days after the
strenuous physical exercise. The ndings of the study conducted by Sjogren, et al., indicated that strength training
and very heavy manual labor are more likely to cause raised in ALT than aerobic exercise. ALT can be elevated in
marathon runners and they have the potential to develop rhabdomyolysis in extreme [28-30].
Finding of the study indicates that mean and standard deviation of AST of CG was 25.35 ± 4.81, mean of EXG
was 27.60 ± 5.35, T-value of both CG and EXG was -1.40, the p-value was 0.170 (t38=1.40, p>0.05). Therefore no
signicant difference was found in AST of both groups CG and EXG. The AST of CG was less than the AST of EXG.
Bakowski, et al., reported that exercise has no effects on liver enzymes such as ALT, ALP, and AST. Although Fallon
and colleagues found a signicant increase in the level of liver enzymes after exercise. They also found that exercise
improve the functional capacity of the liver if it is performed according to the nature and capacity of the body [31,32].
Findings show that mean and standard deviation FRAP of CG was 138.59 ± 21.83, mean of EXG was 120.90 ±
13.45, T-value of both CG and EXG was 3.08, and the p-value was 0.004 (t38=3.08, p<0.05). Therefore a signicant
difference was found in FRAP value of both groups CG and EXG. The FRAP value of CG was higher than the
FRAP value of EXG. Previous studies by Turner, et al., and Berzosa, et al., indicated that low as well as moderate-
intensity exercise causes an increase in oxidative stress in young healthy males if it is performed more according to
the approach of the body [33,34].
Findings indicate that mean and standard deviation FRAP of EXG (A) was 115.25 ± 12.08, mean of EXG (B) was
126.55 ± 12.86, T-value of both EXG (A and B) was 2.02, the p-value was 0.058 (t18=2.02, p>0.05). Therefore no
signicant difference was found in FRAP of both EXG (A) and EXG (B). The FRAP of EXG (A) was less than the
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FRAP of EXG (B). The ndings of the study conducted by Dembinska-Kiec, et al., determine that diet with all its
basics elements strengthen the antioxidants system of the body. Sin, et al., stated that different kind of micronutrients
such as vitamins E and C help to maintain the balance in ROS and antioxidants. Therefore this ndings also seemed
inline of the present study nding [35,36].
CONCLUSION
On the basis of ndings, the researcher concluded that low-intensity exercise has no signicant effects on liver
enzymes. In addition, it was also concluded that low-intensity exercise helps in the improvement of blood life quality
by reducing various health problems related to oxidative damages of cells and muscles fatigue.
REFERENCES
[1] Urso, Maria L., and Priscilla M. Clarkson. “Oxidative stress, exercise, and antioxidant supplementation.”
Toxicology, Vol. 189, No. 1-2, 2003, pp. 41-54.
[2] Sen, Amartya. “Social exclusion: Concept, application, and scrutiny.” 2000.
[3] Sabo, Arianna, et al. “Selective transcriptional regulation by Myc in cellular growth control and lymphomagenesis.”
Nature, Vol. 511 No. 7510, 2014, p. 488.
[4] Spaan, Willy, et al. “Coronavirus mRNA synthesis involves the fusion of non‐contiguous sequences.” The
EMBO Journal, Vol. 2, No. 10, 1983, pp. 1839-44.
[5] Dellinger, R., Phillip, et al. “Surviving Sepsis Campaign: international guidelines for the management of severe
sepsis and septic shock: 2008.” Intensive Care Medicine, Vol. 34 No. 1, 2008, pp. 17-60.
[6] Druker, Brian J., et al. “Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.” New
England Journal of Medicine, Vol. 355, No. 23, 2006, 2408-17.
[7] Wadley, Alex J., Jet JCS Veldhuijzen van Zanten, and Sarah Aldred. “The interactions of oxidative stress and
inammation with vascular dysfunction in aging: the vascular health triad.” Age, Vol. 35 No. 3, 2013, pp. 705-18.
[8] Urso, Maria L., and Priscilla M. Clarkson. “Oxidative stress, exercise, and antioxidant supplementation.”
Toxicology, Vol. 189, No. 1-2, 2003, pp. 41-54.
[9] Villeneuve, Daniel L., et al. “Altered gene expression in the brain and ovaries of zebrash (Danio rerio) exposed
to the aromatase inhibitor fadrozole: microarray analysis and hypothesis generation.” Environmental Toxicology
and Chemistry, Vol. 28, No. 8, 2009, pp. 1767-82.
[10] Halliwell, Barry, and John M. C. Gutteridge. “[1] Role of free radicals and catalytic metal ions in human disease:
an overview.” Methods in Enzymology. Academic Press, Vol. 186, (1990), 1-85.
[11] Cooper, C. E., et al. “Exercise, free radicals, and oxidative stress.” Biochemical Society Transactions, Vol. 30,
2000, pp. 280-85.
[12] den Hollander, Anneke I., et al. “Leber congenital amaurosis and retinitis pigmentosa with Coats-like exudative
vasculopathy are associated with mutations in the crumbs homologue 1 (CRB1) gene.” The American Journal of
Human Genetics, Vol. 69, No.1, 2001, pp. 198-203.
[13] Hakim, A. A., et al. Effects of walking on mortality among non-smoking retired men. New England Journal of
Medicine, Vol. 338, No. 2, 1998, pp. 94-99.
[14] Warburton, Darren E. R., Crystal Whitney Nicol, and Shannon S. D. Bredin. “Health benets of physical activity:
the evidence.” Canadian Medical Association Journal, Vol. 174, No. 6, 2006, pp. 801-09.
[15] Oppmann, Birgit, et al. “Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities
similar as well as distinct from IL-12.” Immunity, Vol. 13, No. 5, 2000, pp. 715-25.
[16] Banerjee, Abhijit V., and Esther Duo. “Inequality and growth: What can the data say?.” Journal of Economic
Growth, Vol. 8, No. 3, 2003, pp. 267-99.
[17] Alessio, Helaine M., et al. “Generation of reactive oxygen species after exhaustive aerobic and isometric exercise.”
Medicine and Science in Sports and Exercise, Vol. 32, No. 9, 2000, pp. 1576-81.
[18] Bailey, Robert C., et al. “Male circumcision for HIV prevention in young men in Kisumu, Kenya: a randomized
controlled trial.” The Lancet, Vol. 369, No. 9562, 2007, pp. 643-56.
8(7): 148-155
Khan, et al. Int J Med Res Health Sci 2019,
143-150
155
Kadhim, et al.
[19] Brito, Jerry, Houman B. Shadab, and Andrea Castillo O’Sullivan. “Bitcoin nancial regulation: Securities,
derivatives, prediction markets, and gambling.” Columbia Science and Technology Law Review, 2014.
[20] De Wilde, A. N. N. I. K., et al. “On the xation of needle biopsies of rat liver tissue as a model to study the ne
structure of sinusoidal cells.” The Kupffer Cell Foundation, 1982, pp. 85-92.
[21] Schwemmer, M., et al. “How urine analysis reects oxidative stress-nitrotyrosine as a potential marker.” Clinica
Chimica Acta, Vol. 297, No. 1, 2000, pp. 207-16.
[22] Powers, Scott K., and Karyn Hamilton. “Antioxidants and exercise.” Clinics in Sports Medicine, Vol. 18, No. 3,
1999, pp. 525-36.
[23] Bloomer, Richard J., et al. “Effects of acute aerobic and anaerobic exercise on blood markers of oxidative stress.”
The Journal of Strength and Conditioning Research, Vol. 19 No. 2, 2005, pp. 276-85.
[24] Powers, Scott K., et al. “Dietary antioxidants and exercise.” Journal of Sports Sciences, Vol. 22, No. 1, 2004,
pp. 81-94.
[25] Radovanović, Dragan S., and Goran Ž. Ranković. “Oxidative stress, stress proteins, and antioxidants in exercise.”
Acta Medica Medianae, Vol. 43 No. 4, 2004, pp. 45-47.
[26] George, Steven M. “Atomic layer deposition: an overview.” Chemical Reviews, Vol. 110, No. 1, 2009, pp. 111-31.
[27] Meyer, C., et al. “The MLL recombinome of acute leukemias in 2013.” Leukemia, Vol. 27, No. 11, 2013, p. 2165.
[28] Statland, B. E., Winkel, P., and Bokelund, H. Factors contributing to the intra-individual variation of serum
constituents: 2. Effects of exercise and diet on the variation of serum constituents in healthy subjects. Clinical
Chemistry, Vol. 19, No. 12, 1973, pp. 1380-83.
[29] Pettersson, Andreas, et al. “Age at surgery for undescended testis and risk of testicular cancer.” New England
Journal of Medicine, Vol. 356, No. 18, 2007, pp. 1835-41.
[30] Saxena, Richa, et al. “Genome-wide association analysis identies loci for type 2 diabetes and triglyceride
levels.” Science, Vol. 316, No. 5829, 2007, 1331-36.
[31] Choueiri, Toni K., et al. “Efcacy of sunitinib and sorafenib in metastatic papillary and chromophobe renal cell
carcinoma.” Journal of Clinical Oncology, Vol. 26, No. 1, 2008, pp. 127-31.
[32] Alkire, M. T., R. J. Haier, and Fallon J. H.. “Toward a unied theory of narcosis: brain imaging evidence for a
thalamocortical switch as the neurophysiologic basis of anesthetic-induced unconsciousness.” Consciousness
and Cognition, Vol. 9, No. 3, 2000. pp. 370-86.
[33] Roger, Véronique L., et al. “Heart disease and stroke statistics-2011 update: a report from the American Heart
Association.” Circulation, Vol. 123, No. 4, 2011, pp. e18-e209.
[34] Berzosa, C., et al. “Acute exercise increases plasma total antioxidant status and antioxidant enzyme activities in
untrained men.” BioMed Research International, 2011.
[35] Herrera Dutan, Edgar Vinicio, and Natali Estefanía Poveda Tapia. “Evaluation of the inhibitory activity of
enzymes A and B glucosidase in fruits of the southern Ecuadorian highlands.” BS Thesis, 2018.
[36] Vestbo, Jørgen, et al. “Global strategy for the diagnosis, management, and prevention of chronic obstructive
pulmonary disease: GOLD executive summary.” American Journal of Respiratory and Critical Care Medicine,
Vol. 187, No. 4, 2013, pp. 347-65.
8(7): 148-155
