الفهرس 
OXIDANT AND ANTIOXIDANT (REDOX) HOMEOSTASISOnly 14 pages are availabe for public view
Abstract
I
ron deficiency anemia is the most common cause of anemia in the world, its prevalence in the developing countries is three to four times higher than that in the developed countries and is usually attributed to inadequate nutrition.
Iron is necessary for maintaining normal structure and function of virtually all mammalian cells and is also involved in the immune and non immune host defense. Iron deficiency causes tissue hypoxia, deficiencies of many iron dependent enzymes and heme containing proteins, and is known to produce many systemic abnormalities.
Oxidative stress plays an important role in the pathogenesis of IDA by prooxidant and antioxidant balance in favor of the prooxidant, leading to potential damage and increased oxidative stress.
A network of antioxidant defense mechanism is present in the body. They are often reducing agents, which exist both intracellularly and extracellularly and have the capacity to react with free radicals and reactive species, minimizing their actions and, thus, delaying or preventing oxidative stress.
Glutathione is a crucial component of the antioxidant defense mechanism and it functions as a direct reactive free radical scavenger. Glutathione s transferase (GST) is an enzyme involved in anti oxidant defense and also involved in detoxication.
The determination of erythrocyte GST activity is a promising indicator of oxidative stress conditions that occur in various types of anemia including iron deficiency anemia.
So, the present study aimed to determine the oxidative stress state in infants with iron deficiency anemia and the effect of oral iron therapy persay and with addition of antioxidant vitamins in the reversal of this state through assessing the serum GST levels as an antioxidant marker.
This study was conducted on 30 infants with iron deficiency anemia (group A) ranged in age from (4 to 24 months) with a mean of (13.3 ± 5.77 months) and 20 healthy infants (group B) in the same age group serving as controls. They were recruited from the outpatient clinic & inpatient department in Pediatrics Hospital of Ain Shams University & Health Insurance Hospital (6th of October) during the period from November 2012 to May 2013.
All the studied infants were subjected to careful history taking laying stress on (personal, family, dietetic and present illness histories), complete clinical examination with special emphasis on (complexion, anthropometric measurement, clinical criteria of anemia and signs of rickets) and laboratory investigation including complete blood count, reticulocytic count, serum iron and serum glutathione s transferase.
Infants with iron deficiency anemia (patients group A) were randomly subdivided into two groups (A1 & A2), group A1 (15 infants) received oral iron therapy for 30 days while group A2 (15 infants) received oral iron and antioxidant vitamins (A + E) (the daily requirement dose) for 30 days. Then both groups of anemic infants (A1 & A2) were reassessed after 30 days of treatment by repeating the following labs; complete blood count, reticulocytic count and serum glutathione s transferase.
The results of this study showed that compared to controls (group B), patients (group A) had a lower weight (significantly) and a lower length (insignificantly) in consideration to anthropometric measurements.
Patients (group A) had a significantly lower Hb level, blood picture parameters (MCV, MCH) and serum iron level compared to controls (group B).
Iron deficiency anemia (IDA) was attributed to bad dietary habits reported in all patients and parasitic infestation that was reported in 43.3% (22/30) of patients.
The results also showed that group (A) patients had a relatively lower mean serum GST level (pre treatment) compared to control group (B) and this was mostly attributed to the chronicity of the condition that resulted in GST consumption.
Post treatment for 30 days both groups of patients (A1 & A2) showed a significant rise in the mean values of their blood picture parameters. Addingly, the mean value of Hb was relatively higher in group A2 (received oral iron and antioxidant vitamins treatment) in comparison to group A1 (received oral iron treatment) though was not statistically significant.
Post treatment, the mean GST value was higher in patients compared to controls and this was explained by the fact that relative alleviation of oxidative stress gets GST levels back to the adaptive response state (i.e. rise to stress).
In addition, comparing group A1 and group A2 patients post treatment, serum GST level was significantly higher in group A2 raising the value of adding the antioxidants to iron therapy in deminishing the oxidative stress state in iron deficiency anemia.
Three patterns of serum GST were detected (incremental, plateau and decremental) according to the changes observed in serum GST levels pre and post treatment for each patient in both groups (A1 & A2) regardless of their absolute numerical value.
So, it was concluded that iron deficiency anemia (IDA) causes an oxidative stress recorded by a low serum GST level in chronic cases due to its consumption followed by its rise post treatment with oral iron therapy persay and a higher rise with combined oral iron and antioxidant vitamins (A & E) therapy.
In addition, the combined therapy causes a rapid correction of the anemic state.