Abstract
Among the different mechanisms involved in oxidative stress, protein carbonylation and lipid peroxidation are both important modifications associated with the pathogenesis of several diseases, including cancer. Hematopoietic cells are particularly vulnerable to oxidative damage, as the excessive production of reactive oxygen species and associated lipid peroxidation suppress self-renewal and induce DNA damage and genomic instability, which can trigger malignancy. A richer understanding of the clinical effects of oxidative stress might improve the prognosis of these diseases and inform therapeutic strategies. The most common protein carbonylation and lipid peroxidation compounds, including hydroxynonenal, malondialdehyde, and advanced oxidation protein products, have been investigated for their potential effect on hematopoietic cells in several studies. In this review, we focus on the most important protein carbonylation and lipid peroxidation biomarkers in hematological malignancies, their role in disease development, and potential treatment implications.
Highlights
Oxidative stress can be defined as an imbalance between the production of reactive oxygen species (ROS) and the ability of the cells to detoxify them [1]
Lymphoma other than HL are covered by the general term non-Hodgkin lymphoma (NHL), which again comprises a heterogeneous group of B-cell and T-cell neoplasms [83,84]
Analysis of the lipid peroxidation products MDA and nitrite revealed significantly higher levels in patients with Myelodysplastic syndromes (MDS) and iron overload (IOL) compared with peers without IOL and the control group, and both parameters positively correlated with the levels of ferritin [41] (Figure 3)
Summary
Oxidative stress can be defined as an imbalance between the production of reactive oxygen species (ROS) and the ability of the cells to detoxify them [1]. The indirect mechanism of protein carbonylation involves the carbonylation of lysine, cysteine, and histidine, which may be caused by their reaction with reactive carbonyl groups produced during the oxidation of carbohydrates (e.g., glyoxal (GO), methylglyoxal (MGO)) and lipids (e.g., HNE, MDA or acrolein (ACR)). This process of carbonyl generation is termed glycoxidation (the formation of advanced glycation end-products (AGEs)) and lipoxidation (the formation of ALEs), respectively [13,14,15,16,17,18]. We consider the experimental groups treated with 4 and 8 mg As2O3/kg body weight
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