Abstract
Objectives: Thalassemia with frequent blood transfusion was considered under oxidative stress because of the chance of iron overload. Patients with thalassemia trait with no blood transfusion might also suffered from oxidative stress because of increased iron metabolism. This pilot study was to investigate if patients of alpha or beta thalassemia trait and received no blood transfusion were suffered from oxidative stress in term of DNA damage in peripheral leucocytes. Method: Comet assay was used to measure DNA damage of 20 normal subjects, 8 alpha and 12 beta thalassemia patients who did not received blood transfusion. The baseline and UV-mediated DNA damages of peripheral white blood cells were measured. The degree of DNA damage was quantified by visual scoring under light microscope after staining with Giemsa stain. Results: The mean (± standard deviation) comet score for normal baseline samples was 8.3 ± 6.1 whereas 105.4 ± 15.7 and 69.8 ± 20.3 for alpha and beta thalassemia respectively. While the comet scores were 71.9 ± 19.6, 193.1 ± 21.8 and 211.8 ± 51.6 for normal, alpha and beta thalassemia samples respectively in UV-treated samples. Results showed that both alpha and beta thalassemia patients had higher leucocytic DNA damage in baseline and oxidative stressed samples. Conclusion: Our data suggested thalassemia patients were under oxidative stress even no iron over loaded through transfusion.
Highlights
DNA damage can be caused by reactive species, radiation, and other chemicals (De Boer et al, 2002; Jackson and Bartek, 2009)
Oxidative DNA damage could be induced by natural metabolic by-products in our body or from the environment (Cadet & Davies, 2017)
Since age is positively associated with DNA damage of peripheral white blood cells, average age of normal subject were kept higher or equal to the thalassemia group
Summary
DNA damage can be caused by reactive species, radiation, and other chemicals (De Boer et al, 2002; Jackson and Bartek, 2009). Reactive oxygen species (ROS) are common cause of DNA damage. They can be the natural byproduct of oxygen metabolism inside our body. The oxidative imbalance increases damage of DNA which may cause genomic instability which is the concern of cancer and ageing (Petr et al, 2020). Chronic diseases, such as hemochromatosis and diabetes, are suggested to relate to oxidative stress and associated with DNA damage (Galaris & Pantopouos, 2008; Szeto & Yeung, 2021)
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