Lipid peroxidation is a well-established indicator of oxidative stress in cells and tissues . Lipid peroxides are unstable and decompose to form a series of compounds, including MDA and 4-HDA, and the measurement of MDA + 4-HDA has been used as an indicator of LPO [20, 21].
In our study, we demonstrated increased LPO in the studied group of hypothyroid patients in comparison with the control group of patients with normal thyroid function. Our results are similar to those reported by Dumitriu et al., who found serum MDA level significantly higher in hypothyroidism when compared with the control group of euthyroid patients . Furthermore, two independent groups described significant reduction of increased serum MDA levels after treatment of hypothyroidism with the use of levothyroxine [11, 12]. Also Konukoğlu et al. found that increased LPO, when measured by thiobarbituric acid reactive substance (TBARS) method, was significantly reduced after treatment with levothyroxine . The increased LPO level observed in both overt and subclinical hypothyroidism was recently explained by the insufficient increase in the antioxidant status, as well as by the altered lipid metabolism .
The main finding of the present study is that we did not demonstrate any additive effect of ablative doses of 131I on serum LPO in hypothyroid patients. Our results contrast with those reported by Konukoğlu et al., who observed higher MDA levels in erythrocyte membranes 2 days after treatment with 131I in patients after subtotal thyroidectomy treated with 3.7 - 5.55 GBq 131I . This apparent discordance may be explained by the high radiation sensitivity of bone marrow producing erythrocytes, the phenomenon which does relate to the present study. In turn, Wolfram et al. observed significant increase in isoprostane level in compartments such as blood plasma or serum and urine, shortly after radioiodine treatment in thyroid cancer patients . As isoprostanes result from oxidation of low-density lipoprotein present in blood, whereas MDA + 4-HDA, evaluated in the present study, result from oxidative damage to membrane lipids of different tissues and organs, which thereafter are "released" into the blood, the values of these two parameters may change even divergently .
Also the following hypothesis to explain the apparent inconsistency between our results and those of other authors should be taken into consideration. It is known that total body irradiation after 131I administration rises with increasing whole-body retention time of radioisotope . As no dosimetric data are available for patients studied by Konukoğlu et al., Bartoc et al., as well as Wolfram et al., it can be speculated that lower thyroid remnants 131I uptake and shorter whole-body retention time of 131I in our patients resulted in lower irradiation of tissues, and, as a consequence, lower LPO [18, 23, 24]. However, in the opinion of the authors of the present study, such a mechanism does not play an essential role.
The negative correlation between radioiodine dose and LPO level, observed in the present study early after radioiodine treatment was not expected. However, this relationship may be explained by well documented protective effects of ionizing radiation used in comparatively low doses [17, 26]. Low doses of ionizing radiation, as well as low doses of any other prooxidant, stimulate intracellular protective mechanisms, antioxidative enzymes included . It is worth stressing that in the present study LPO level decreased slightly within the first two days after radioiodine treatment and that this decrease would be possibly statistically significant in case of much lower baseline value (such as in the control group). Huge increase in LPO level due to severe hypothyroidism made impossible to clearly reveal the decrease in LPO level due to radioiodine treatment. However, this hypothesis should be experimentally proved, for example by measurement of other indices of oxidative damage to macromolecules. Nevertheless, the negative correlation between radioiodine dose and LPO level early after radioiodine treatment intensifies the main finding of the present study, showing that ablative doses of 131I do not induce significant peroxidation of membrane lipids in thyroid cancer patients within the first days of therapy. This finding is of great clinical importance and relates especially to those thyroid cancer patients, who are not treated with recombinant TSH, thus being hypothyroid not only before but also shortly after radioiodine therapy.
It is concluded that radioiodine remnant ablation of differentiated thyroid cancer does not further increase oxidative damage to membrane lipids, at least early, i.e. within the first 4 days, after therapy.