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Short Communication
Rev Bras Hematol Hemoter. 2012;34(5):394-5
Leukocyte superoxide dismutase activity in patients with chronic myeloid leukemia
Introduction
Chronic myeloid leukaemia (CML) is a myeloproliferative disorder of the hematopoietic
cell and is associated with a characteristic chromosomal translocation called the Philadelphia
chromosome. Clinically, CML is often divided into three phases; CML typically begins in
the chronic phase (CML-CP) and in the absence of intervention and over the course of
several years progresses to an accelerated phase (CML-AP) and ultimately to blast crisis.
Blast crisis is the terminal phase of CML and clinically behaves like acute leukemia
(1)
. Free
radicals can be key contributory agents in a number of human diseases, including cancer
and leukaemia
(2,3)
. These free radicals can be generated within the cell not only by external
sources of radiation but also within the body as a by-product of normal metabolic processes
which include the electron transport chain, drugs, pollutants, and chemicals including
toxins, collectively termed as xenobiotics. Thus, antioxidants which balance the oxidative
stress state represent a major line of defense in regulating the overall true state of health
(2)
.
Antioxidant enzymes such as superoxide dismutase (SOD) can directly counter the oxidants
and may protect cells against oxidative stress. Studies show that cancer cells have abnormal
activities of SOD enzymes when compared to an appropriate normal counterpart. There
are no available publications regarding the relationship between leukocyte SOD enzyme
activity in CML and its progression. The present study was planned to propose leukocyte
SOD activity as a possible biomarker for oxidative stress in CML and its correlation with
the progressive phases of CML.
Methods
This study included 83 CML patients and 50 age- and gender-matched healthy volunteers.
Leukocyte SOD activity was measured by the spectrophotometric method
(4)
.
Results
At the time of diagnosis, the mean leukocyte SOD activity in CML, CML-CP and
CML-AP were significantly higher (p-value < 0.001, p-value < 0.01 and p-value < 0.001,
respectively) than in healthy volunteers (Table 1). CML-CP patients who converted into
CML-AP had significantly higher (p-value < 0.05) leukocyte SOD activity than CML-CP
patients who did not convert into CML-AP (Table 2).
Rizwan Ahmad
Ranjana Singh
Anil Kumar Tripathi
Raj Kumar Singh
King George’s Medical University, Chowk,
Lucknow, India
Conflict-of-interest disclosure:
The authors declare no competing financial
interest
Submitted: 8/31/2012
Accepted: 9/4/2012
Corresponding author:
Raj Kumar Singh
Biochemistry Department, Shri Guru
Ram Rai Institute of Medical & Health
Sciences,
Patel Nagar
248001 Dehradun, Uttarakhand, India
singhrk23a@hotmail.com
www.rbhh.org or www.scielo.br/rbhh
DOI: 10.5581/1516-8484.20120097
Table 1 - Leukocyte superoxide dismutase activity in CML, CML-CP,
CML-AP patients and healthy subjects
Groups
n
Leukocyte SOD activity
(U/mg protein)
Healthy Subjects
50
11.69 ± 4.34
CML
83
16.99 ± 7.61**
CML-CP
62
15.94 ± 7.52***
CML-AP
21
19.94 ± 7.26**
CML: Chronic myeloid leukaemia; CML-CP: Chronic myeloid leukaemia - chronic phase;
CML-AP: Chronic myeloid leukaemia - accelerated phase; SOD: superoxide dismutase
Values are mean ± SD; **p value < 0.0001; ***p value < 0.001