Abstract
Intravascular hemolysis is a fundamental feature of hemorrhagic venereal infection or tissue and releases the endogenous damage-associated molecular pattern hemoglobin (Hb) into the plasma or tissues, which results in systemic inflammation, vasomotor dysfunction, thrombophilia, and proliferative vasculopathy. However, how the cytotoxic Hb affects the tissues of grass carp remains unclear. Here, we established a hemolysis model in grass carp by injecting phenylhydrazine (PHZ). The data revealed that the PHZ-induced hemolysis increased the content of Hb and activated the antioxidant system in plasma. The histopathology analysis data showed that the PHZ-induced hemolysis increased the accumulation of Hb and iron both in the head and middle kidney. The results of quantitative real-time PCR (qRT-PCR) detection suggested that the hemolysis upregulated the expressions of iron metabolism-related genes. In addition, the immunofluorescence and immunohistochemistry data revealed that the hemolysis caused an obvious deposition of collagen fiber, malondialdehyde (MDA), and 4-hydroxynonenal (4-HNE) accumulation and increased the content of oxidative-related enzymes such as β-galactosidase (β-GAL), lipid peroxide (LPO), and MDA in both the head and middle kidney. Furthermore, the PHZ-induced hemolysis significantly increased the production of reactive oxygen species (ROS), which resulted in apoptosis and modulated the expressions of cytokine-related genes. Taken together, excess of Hb released from hemolysis caused tissue oxidative damage, which may be associated with ROS and inflammation generation.
Highlights
Hemoglobin (Hb) is an iron-containing metalloprotein whose main biological function is oxygen transport
To assess whether hemolysis in grass carp affects the antioxidant system, we determined the activity of three antioxidases: glutathione peroxidase (GSH), superoxide dismutase (SOD), and catalase (CAT)
Compared to GSH, we observed a significantly increased effect on the SOD contents at all tested time points (Figure 1D)
Summary
Hemoglobin (Hb) is an iron-containing metalloprotein whose main biological function is oxygen transport. Under normal circumstances, it is sequestered in the erythrocytes by a highly efficient antioxidant system to prevent vasculature or other tissues from exposure to this pro-oxidative and proinflammatory protein [1, 2]. Excessive high oxidation activity and the pro-inflammatory effects of Hb or heme can overwhelm and impair antioxidants and result in oxidative damage, such as protein oxidation, lipid peroxidation, and nucleic acid oxidation, leading to cellular dysfunction and cell death [6, 16]. Studies revealed that intravascular hemolysis and the subsequent release of pro-inflammatory Hb and heme into circulation or tissues are characteristic of several human diseases, including sickle cell disease (SCD), thalassaemias, spherocytosis, paroxysmal nocturnal hemoglobinuria (PNH), autoimmune hemolytic anemia (AIHA), thrombotic microangiopathy (TMA), acute kidney injury (AKI), chronic kidney disease, and atypical hemolytic uremic syndrome (aHUS), among others [11, 17–21]
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