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Effect of desferal drug and green tea on the levels of lipid prophile in sera of rabbits induced diabetes mellitus by iron overload.


Iron and iron overload catalytic ability lies in the redox activity of iron, which is able to cycle between two stable configurations, ferric ([Fe.sup.+3]) and ferrous ([Fe.sup.+2]) states, allowing it to act as an electron donor and acceptor. The biological importance of iron is due to its participation in the oxidation-reduction process known as the HaberWeiss reaction (equation 3)

[Fe.sup.3+] + [O.sup.*.sub.2] - [right arrow] [Fe.sup.2] + [O.sub.3] .... .... .1

[Fe.sup.2] + [H.sub.2] [O.sub.2] - [right arrow] [Fe.sup.3] + [OH.sub.-] + [O.sup.*] H .... .... .2


Ferritin (iron store within ferritin in the oxidized form [Fe.sup.+3]) is reduced when iron availability is low, contributing to overall iron homeostasis of iron within ferritin is critical for prevention of (ROS) formation, protecting the cell from oxidative damage. [1,2].

Iron with green tea

Both green and black teas are also potent inhibitors of intestinal absorption of non-heme iron, lowering the amount of free iron reaching the brain in the first place. There is also some evidence that iron plays a part in epilepsy. Green tea polyphenols have been found to inhibit or diminish iron-induced epileptic seizures, and to inhibit hyperactivity of dopaminergic neurons, it is in fact likely that green tea as especially the decaffeinated kind, acts a mild sedative [3,4].

Desferal drug

Iron overload may be treated or prevent with a chelating agent such as desferrioxamine (DFO) which is capable of complexing with iron and promoting its excretion. Iron bound by DFO is rendered virtually inactive: hence, the drug can prevent or reverse the effects of free radical formation and lipid peroxidation [5].

Area Of Study

To compare the treatment between Green tea and Desferal in sera of rabbits induced with diabetes mellitus.

Experimental Animals

The experimental animals (male domestic rabbits Oryctalagus Cuniculus) were treated as following:

Rabbits Housing

Fourteen male rabbits (1.9-2.2) Kg body weight and (4-6) months of age were purchased from local market. The rabbits (2 rabbits/cage) housed under controlled animal conditions of temperature (25 [+ or -] 3 C[degrees]) and relative humidity (50 [+ or -] 5)%. Upon arrival, animals were adapted for two weeks and were maintained on a regular feed (control diet) consist of alfalfa and concentrate pullet (Crude protein 10%, ground soybean 20%, wheat flour 35%, corn 35%, mineral & vitamins 1 gm/Kg). Total energy was 13.6 Kj/Kg protein. The rabbits were divided into Two groups. The control group (n=5) was fed the control diet.

Iron overload group (IO) (n=9) were fed the control diet in addition to give iron gluconate (ferrosam) by oral administration. The doses of iron gluconate ~0.2 ml/Kg/d were given during the last month from the experiment that went on three months. The total dose equal (100 mg), divided into 20 mg/d doses for 5 days.[6,7].


Treatment for Iron overload nine rabbits were allocated randomly into two groups:--

Group 1: (n=5) fed orally 5% green tea dissolved in double distilled water [8].

Group II: (n=4).injected Desferal subcutaneously as their regular chelation therapy 10 mg/kg. Desferal administrated two to three times per week achieves iron excretion greater than induced by daily deferiprone [9]

Materials and Methods

Biochemical measurements:

Some biochemical measurements to make out by using special enzymatic kits were performed as in the following:

* Total cholesterol Determination

* Determination of serum triglyceride

* Measurement of serum lipoprotein cholesterol

1. High-density lipoprotein (HDL)

2. Very low density lipoprotein (vLDL).

3. Low-density lipoprotein (LDL).

* Determination of serum Malondialdehyde [10].

* Determination of serum reduced glutathione [10].

* Determination of ascorbic acid (vitamin C) [11].

* Determination of Blood-Glucose [11].

* Determination of vitamin E [12].

* Determination of serum iron by using a linear chemical kit (France).

* Total Iron Binding Capacity (TIBC) by using a linear chemical kit (France).

* Determination of serum-copper & zinc by Atomic Absorption Technique.[13].

* Determination of serum uric acid and allantoin by HPLC Technique [14].

Results and Discussion

Glutathione (GSH) levels

In Iron overload groups, the levels of reduced serum glutathione (GSH) were significantly decreased (0.02) before treatment comparing with control and significantly increased (0.014) after treatment with green tea, and the value was very significant (P<0.000) after treated by desferal, Table (1).

In iron overload group, the levels of Vit.C were significantly decreased (p=0.03, p=0.027) before and after treatment with desferal. Reduced levels of serum vitamin C in diabetic patients could be due to increased oxidative stress [15]. Ascorbic acid depletion results from irreversible oxidation of ascorbic acid by iron. In ascorbic acid synthesizing species such as the rat, the decreased plasma levels of ascorbic acid may be that iron overload affected the rate of ascorbic acid synthesized in the liver [16].

Iron overload in human is associated with significantly decreased plasma ascorbate levels suggesting that high iron levels enhance the rate of ascorbate catabolism [17]. However Vitamin C administration enhances the removal of iron by desferoxamin and increases transferrin saturation and ferritin levels [18]. While in other study, no correlation was seen with antioxidant capacity because it was present in low amounts in most samples [19] and on increasing dietary ascorbic acid no improved iron status was seen. High in phytate and non heme iron were seen in iron--deficient women consuming diets, [20].

Vitamin E ([alpha]-tocopherol)

Serum vitamin Eisa principal modular of free radicals activity; it is a potent antioxidant acting as scavenger of reactive oxygen species (ROS) and reduces oxidative stress. The level of Vit.E was significantly decreased after handling with ferrosam (p<0.05). Table. (1)

The present study showed that dietary IO led to a marked decreased in serum [alpha]-tocopherol levels agree with previous data [16]. Vitamin E supplements could fully prevent iron -induced lipid peroxidation. Also correction of impaired vitamin C status may protentiate the vitamin E effect through regeneration of vitamin E from the vitamin E radical formed during the antioxidation action of vitamin E [21,22].

Iron and other indices of Iron Metabolism:--total iron binding capacity and transferring saturation% (Tsat %):

After handling with ferrous gluconate the (iron and Tsat%) were significantly increased (p<0.05) and TIBC was insignificant, but with desferal treatment both of TIBC and Tsat% were significantly decreased (p<0.000, p=0.004). While the levels of iron did not change p>0.1. The (iron, TIBC and Tsat%) were significantly decreased after treatment with green tea (p<0.000). Table (2). The rabbits with oral iron gluconate administration were treated because the intravenous (iv) iron administration may be associated with severe side effect attributable to inflammation and/or hyperoxidation as consequences of local effect of free iron. In humans, iron overload conditions are usually associated with increased Serum Iron (SI) level and decreased TIBC. The present results were in agreement with other studies [23,24].

Trace elements (Copper and Zinc)

After handling with ferrous gluconate the level of copper was significantly decreased (p<0.000), while the level of zinc had insignificant differences. The level of zinc was significantly decreased (p=0.016) after treatment with desferal, while the level of copper had insignificant differences. Both of them were significantly decreased (p<0.000, p=0.017) after treatment with green tea, Table (2). Zinc administration, which inhibits lipid peroxidation and increases glutathione availability by preventing the oxidation of glutathione also, has ability to inhibit the uptake of iron [25]. Patients with IO receiving DFO only those with DM had significantly increased urinary zinc excretion compared with normal [26]. Gruen et al., [27], found that serum liver and heart copper concentrations were decreased in association with increased iron concentration in these tissues suggested that decreases in copper concentration with the resultant decreases in ceruloplasmin levels may be a contributing factor in the increase of hepatocyte iron, as noted by [28].

Lipid profile

Increasing protein content in diet for 15-30% of the total energy, while carbohydrate content decreases, this can results in no significant differences of the total cholesterol, low density lipoprotein, and high density lipoprotein levels. A lowered levels of triglyceride has been formed to be significant (P<0.05)[29]. In Iron overload group and after treated by desferal, total cholesterol, and HDL-C levels were significantly increased p<0.01 and p<0.001, while the level of LDL-C, and TG were significantly decreased p<0.000 and p<0.01. After treatment with green tea, the level of TC and LDL-C were significantly decreased p < 0.000, while the levels of HDL-C and TG were significantly increased p<0.000 and p=0.0249 Table (3): (Mean [+ or -]SD&P- test) of lipid profile in the healthy rabbits control and iron overload before and after treatment with DFO.

Animal studies on the role of iron in experimental atherosclerosis are limited and also have yielded conflicting results. Although one study suggested that excessive iron loading in hypercholesterolemic rabbits was beneficial and significantly reduced lesion formation),a similar study suggested a detrimental role for iron loading in the same model [30,31]. Excessive iron induces cellular injury and functional abnormalities in hepatocytes by the process of lipid peroxidation [32]. Lipid peroxidation may also damage membranes in other cells, altering important elements such as increased LDL cholesterol (LDL-C), and decreased HDL--cholesterol (HDLC) [31,33] treated rabbits with iron dextran and did not find differences in plasma cholesterol between groups fed a high cholesterol and control diet. Experiments with rats were only considered, there was consensus that excess iron increases HDL-C as was observed by[16], with rats that consumed a diet containing cholesterol with rats that were fed a diet without cholesterol. Dabbagh et al.,[16] found an increase in total cholesterol and triglycerides, where as in other work showed a reduction in serum cholesterol and no effect on serum triglycerides [33].

Malondialdehyde (MDA):

Dien conjugation (DC)and thiobarbituric acid reactive species (TBARS) are widely used as indicators of lipid peroxidation .DC is a measure of early events of lipid peroxidation reactions whereas TBARS measure end product of lipid peroxidation, malondialdehyde (MDA), that is a goal marker of cell membrane damage following ROS production during stress [34]. Study illustrated by [21] showed that MDA concentration did not increased in the absence of iron application but showed a significant decrease at an approximate rate of 0.03 ([micro]mole/L/h) within 180 min, this decreases did not result from plasma volume changes but rather from elimination of MDA by hemodialysis treatment because of its relatively low molecular mass. In rodents, MDA became rapidly distributed through out all major organs and acid-- labile MDA metabolites, with very little free MDA were excreted in urine [35].

Antioxidant vitamins act as quencher for free radicals, thus, increased levels of serum antioxidant vitamins could be reduce the level of MDA, the end product of lipid peroxidation. The new trend in the management of diabetes and decrease lipid peroxidation degree is to use therapeutic antioxidant and scavengers like vitamin E and vitamin C [36]. Elevated levels of lipid peroxidation products in serum of diabetic subjects and rats have been shown in several studies [37,38], higher levels of MDA is associated with decreased of antioxidnt activity and increased oxidative stress [39,40]. Elevated level of MDA might increase susceptibility of diabetic patients to cardiovascular complications. Figure (1).

The results of iron overload (IO), MDA levels were positively correlated with HDL (r=0.25, p<0.000), GSH (r=0.0849, p<0.000) & TG (r=0.31, p<0.000) and negatively correlated with LDL (r=-0.228, p<0.000) and B. sugar (r=-0.266, p<0.000). Figure (2). Antioxidant vitamins act as quencher for free radicals, thus, increased levels of serum antioxidant vitamins could be reduce the level of MDA, the end product of lipid peroxidation. The new trend in the management of diabetes and decrease lipid peroxidation degree is to use therapeutic antioxidant and scavengers like vitamin E and vitamin C [36].


Uric acid and Allantoin

In the IO group, the levels of (uric acid, allantoin and blood sugar) were significantly increased (p<0.000, p < 0.000, p < 0.000) after handling with ferrous gluconate, while the levels of them were significantly decreased (p<0.000, p<0.000, p=0.0031) and (p<0.000, p<0.000, p=0.004) after treatment with desferal and green tea respectively. Tab. (3), fig (7, 8, 9).


The results of heamoglobin level was significantly increased (p<0.000) after handling with ferrous gluconate for 1 month and it was significantly decreased (p=0.05) after 1 week treatment with desferal and green tea (p<0.05, p=0.007), while the results indicated that levels of hemoglobin after 2nd and 4t week of treatment with desferal and green tea were insignificantly differ (p>0.05) respectively.Tab. (2) & (4);

In the third group (IO), the results illustrated positive correlation with blood sugar treated by green tea (r=0.453, p<0.000), allantoin treated by DFO (r=0.364, p<0.000) and GSH treated by DFO (r=0.0533, p<0.000) levels and vit.E (r=0.414, p<0.000) levels. Negative correlation with blood sugar treated by desferal, (r=-0.457, p<0.000) allantoin treated by green tea (r=-0.461, p<0.000) and GSH after treated by green tea (r=-0.28, p<0.000) levels.

The results for this study reported different direct correlation between serum uric acid and serum of several parameters such as : allantoin, GSH and vitamin C, where as there was direct correlation but not significant with copper, while the others were significant The direct correlation between serum uric acid and blood sugar after treated by DFO and green tea, vitamin E, and (allantoin and GSH) after treated by DFO, while there were significant negative correlation between uric acid and the levels of allantoin and GSH after treated by green tea).

Uric acid is generated in the human body by the oxidation of purines, but no enzyme is present to oxidize it further. One function of uric acid in human body fluids is to act as an antioxidant, experiments in vitro have been shown that uric acid act to protect erythrocytes against damage singlet oxygen [sup.1][O.sub.2] to inhibit lipid peroxidation, to inhibit oxidative degradation of hyaluronic acid to protect against free - radical damage to DNA and to bind transition-metal ions in complexes that were poorly active in promoting free-radical reactions [41].

The previous studies in rats would increase over all oxidative stress while the result were indicated the opposite, that increased dietary protein in rats significantly decreased measures of oxidative stress [42]. Serum uric acid concentration was not significantly changed in rheumatoid patients, but allantoin concentrations were significantly raised. In both serum and synovial fluid the allantoin / uric acid concentration ratio was raised in rheumatoid. Plasma allantoin has been reported to increase in conditions associated with increased oxidative stress and can be decreased after antioxidant supplementation [41, 43,44 ]. Uric acid was present in low amounts not affected by iron intervention so, IO led to a slight but statistically non significant decrease in plasma uric acid levels [16]. No significant correlation was found between allantoin and urate while urate concentration has been reported to correlate negatively with vitamin E concentration and positively with lipoperoxides as (TBARS) [45]. The redox reaction of uric acid and allantoin levels used to assess the degree of oxidative stress, there was a positive correlation between allantoin level and oxidative stress [46].

The allantoin--uric acid pathway play a critical control point in the reaction of nitric oxide and superoxide anion in cells production uric acid--derived free radical which is possibly prevented by uricase [47]. The activity of uricase enzyme is less than other antioxidant enzymes (Cu-Zn, SOD, Mn-SOD, catalase) in oxidative stress. the metabolic conversion of uric acid to allantoin and thereby reducing the scavenging effect of allantoin [39], therefore both uric acid and allantoin via uricase activity were contributed in protection the myocardium against free radical, but this protection was of rate limiting [48].


The results found in the study enable for concluding the following points:

* The aim of the study by finding the effect of iron overload on causing the diabetic by destruction pancreatic gland and the effect of iron overload when it's chelated with specific chelating agent desferal (DFO).

* The green tea can prevent the effect of iron overload at the same action of desferal.

From the different parameters were affected:

* Decreased antioxidant levels, GSH, Vitamin C , uric acid and allantoin) and copper.

* Increased in blood sugar, serum iron and haemoglobin, while vitamin E and zinc levels were unaffected.

Our finding in hyperproteinemia (HP) SOME PARAMETERS WERE decreased such as (Vitamin E, LDL and copper) and others were increased such as (GSH, Zinc, Vit.C, uric acid and allantoin) while HDL and transferring saturation were unaffected

The observation in diabetic rabbits increment in (MDA, LDL, serum iron, B.sugar, uric acid & allantoin), and decrement in (GSH, HDL, zinc and copper), while the vitamins (C and E) were unaffected.

Decreased levels of GSH, HDL and zinc are the powerful indicators to evaluate the oxidative stress syndrome in diabetic than non-diabetic.


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Oda M. Al-Zamely, Amira M.A. Jasim and * Mufeed J. Ewadh

Department of Chemistry, College of Science, University of Babylon, Babylon, Iraq

* Formally Department of Clinical Biochemistry College of Medicine, University of Babylon, Babylon, Iraq

Table 1: level of several non-enzymatic antioxidants such as (GSH,
vit.C, vit.E & uric acid) Blood sugar and allantoin in serum of
control and Iron overload

 Parameter Control After handling with
 ferrous gluconate

GSH [micro]mole/L 11.3 [+ or -] 8.16 [+ or -] 1.52,
 2.92 p = 0.02

 Vit.C mg/dL 0.01 [+ or -] 0.0064 [+ or -]
 0.0038 0.003, p = 0.14

 Vit.E mg/dL 0.458 [+ or -] 0.404 [+ or -] 0.029,
 0.042 p = 0.048

 Uric acid 3.335 [+ or -] 9.87 [+ or -] 1.06,
 [micro]mole/L 0.685 p < 0.000 48.73 [+ or -]
 After handling 1.38, P < 0.000

 B.sugar mg/dL 104.98 [+ or -] 227.02 [+ or -] 50.47,
 6.785 p < 0.000

 Allantoin 325 [+ or -] 267.85 [+ or -] 26.24,
 [micro]mole/L 87.2 p < 0.000 5196.07 [+ or -]
 after handling 1175.33, p < 0.000

 Parameter Treated by DFO Treated by green tea

GSH [micro]mole/L 14.2 [+ or -] 3.56, 13.75 [+ or -] 5.61,
 p < 0.000 p = 0.014

 Vit.C mg/dL 0.0062 [+ or -] --
 0.0033, p = 0.08

 Vit.E mg/dL -- --

 Uric acid 3.40 [+ or -] 0.36, 2.52 [+ or -] 0.23,
 [micro]mole/L p < 0.000 p < 0.000
 After handling

 B.sugar mg/dL 141.83 [+ or -] 115.52 [+ or -] 13,
 7.04, p = 0.0031 p = 0.004

 Allantoin 281.50 [+ or -] 343.96 [+ or -] 140.6,
 [micro]mole/L 43.57, p < 0.000 p < 0.000
 after handling

Table 2: level of several trace elements (Iron, copper & zinc) with
hemoglobin (Hb) in the serum control and Iron overload.

 Parameter Control After handling with
 ferrous gluconate

 Serum Iron(SI) 21.59 [+ or -] 330.75 [+ or -] 19.79,
 [micro]g/dL 3.88 p < 0.000

 Total Iron Binding 920 [+ or -] 1049.24 [+ or -] 154.68,
 Capacity [micro]g/dL 32.89 p = 0.09

 transferin saturation% 2.33 [+ or -] 31.52 [+ or -] 0.68,
 (Tsat%) 0.344 p < 0.000

 Copper (Cu) ppm 1.18 [+ or -] 0.75 [+ or -] 0.2,
 0.057 p < 0.000

 Zinc (Zn) ppm 0.64 [+ or -] 0.56 [+ or -] 0.13,
 0.13 p = 0.34

 Hemoglobin (Hb) g/L 11.6 [+ or -] 12.6 [+ or -] 0.91,
 0.136 p = 0.005

 Hb after handling for 15.55 [+ or -] 1.02,
 one month p < 0.000

Hb after treatment with
 DFO at 1st week

Hb after treatment with
 DFO at 2nd week

Hb after treatment with
 G Tea at 1st week

Hb after treatment with
 G. Tea at 4th week

 Parameter Treated by DFO Treated by
 Green Tea

 Serum Iron(SI) 189.07 [+ or -] 147.98 [+ or -]
 [micro]g/dL 25.07, p = 0.19 39.5, p < 0.000

 Total Iron Binding 577.69 [+ or -] 615.21 [+ or -]
 Capacity [micro]g/dL 8.75, p < 0.000 22.4, p < 0.000

 transferin saturation% 29.22 [+ or -] 24.05 [+ or -]
 (Tsat%) 3.9, p = 0.004 5.2, p < 0.000

 Copper (Cu) ppm 1. 0 [+ or -] 0.5 [+ or -]
 0.41, p = 0.18 0.07, p = 0.017

 Zinc (Zn) ppm 0.35 [+ or -] 0.21 [+ or -]
 0.108, p = 0.016 0.065, p < 0.000

 Hemoglobin (Hb) g/L -- --

 Hb after handling for
 one month

Hb after treatment with 11.978 [+ or -]
 DFO at 1st week 0.33, p = 0.05

Hb after treatment with 12.04 [+ or -]
 DFO at 2nd week 0.33, p = 0.06

Hb after treatment with 12.028 [+ or -]
 G Tea at 1st week 0.63, p = 0.007

Hb after treatment with 13.33 [+ or -]
 G. Tea at 4th week 0.77, p = 0.13

Table 3: (Mean [+ or -] SD&P-test) of lipid profile in the healthy
rabbits control and iron overload before and after treatment with DFO.

Parameter After Handling Treated by DFO Treated by Green
 Ferrous gluconate Tea

 TC 69.24 [+ or -] 0.83 71.36 [+ or -] 57.83 [+ or -] 2.96,
 5.40, p = 0.1 p < 0.000

 HDL 11.32 [+ or -] 2.69 16.38 [+ or -] 17.72 [+ or -] 0.41,
 1.0, p < 0.001 p < 0.001

 TG 28.62 [+ or -] 3.79 23.68 [+ or -] 31.26 [+ or -] 2.09,
 0.95, p = 0.01 p = 0.0249

 VLDL 5.72 [+ or -] 0.75 4.73 [+ or -] 6.32 [+ or -] 0.41,
 0.19, p = 0.01 p = 0.0249

 LDL 52.19 [+ or -] 2.66 50.24 [+ or -] 33.78 [+ or -] 3.06,
 5.43, p < 0.000 p < 0.000

Table 4: The correlation between the levels of uric acid
[micro]mole/L with other variables in three groups.

 Correlation of Iron overload
 uric acid Correlation coefficient(r)

 r P value

Copper ppm -- --

Allantoin 0.36 DFO
[micro]mole/L -0.46 green tea <0.000 0.0093

Vitamin C mg/dL -- --

GSH [micro]mole/L 0.53 DFO <0.000
 -0.28 green tea <0.000

Blood sugar +0.45 green <0.000
 tea <0.000
 -0.456 DFO
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Author:Al-Zamely, Oda M.; Jasim, Amira M.A.; Ewadh, Mufeed J.
Publication:International Journal of Biotechnology & Biochemistry
Date:Dec 1, 2010
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