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氨基酸补充在恶性疟原虫旁观者应激前对红细胞提供保护。

Amino acid supplementation confers protection to red blood cells before Plasmodium falciparum bystander stress.

机构信息

Department of Biology, Wake Forest University, Winston-Salem, NC.

Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, NC.

出版信息

Blood Adv. 2024 May 28;8(10):2552-2564. doi: 10.1182/bloodadvances.2023010820.

DOI:10.1182/bloodadvances.2023010820
PMID:38537079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11131086/
Abstract

Malaria is a highly oxidative parasitic disease in which anemia is the most common clinical symptom. A major contributor to the malarial anemia pathogenesis is the destruction of bystander, uninfected red blood cells (RBCs). Metabolic fluctuations are known to occur in the plasma of individuals with acute malaria, emphasizing the role of metabolic changes in disease progression and severity. Here, we report conditioned medium from Plasmodium falciparum culture induces oxidative stress in uninfected, catalase-depleted RBCs. As cell-permeable precursors to glutathione, we demonstrate the benefit of pre-exposure to exogenous glutamine, cysteine, and glycine amino acids for RBCs. Importantly, this pretreatment intrinsically prepares RBCs to mitigate oxidative stress.

摘要

疟疾是一种高度氧化的寄生虫病,贫血是最常见的临床症状。导致疟原虫贫血发病机制的一个主要因素是旁观的、未感染的红细胞(RBC)的破坏。已知急性疟疾患者的血浆中会发生代谢波动,这强调了代谢变化在疾病进展和严重程度中的作用。在这里,我们报告来自恶性疟原虫培养的条件培养基可诱导无感染、过氧化氢酶耗尽的 RBC 发生氧化应激。作为谷胱甘肽的细胞可渗透前体,我们证明了预先暴露于外源性谷氨酰胺、半胱氨酸和甘氨酸氨基酸对 RBC 的益处。重要的是,这种预处理从本质上使 RBC 能够减轻氧化应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/2618b8a13375/BLOODA_ADV-2023-010820-gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/a9aecfa5de0e/BLOODA_ADV-2023-010820-ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/e9d1c95ed190/BLOODA_ADV-2023-010820-gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/c2a96b3f6e2f/BLOODA_ADV-2023-010820-gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/0aa8013eb7eb/BLOODA_ADV-2023-010820-gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/5099bf5ee67c/BLOODA_ADV-2023-010820-gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/de38c72db73c/BLOODA_ADV-2023-010820-gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/2618b8a13375/BLOODA_ADV-2023-010820-gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/a9aecfa5de0e/BLOODA_ADV-2023-010820-ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/e9d1c95ed190/BLOODA_ADV-2023-010820-gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/c2a96b3f6e2f/BLOODA_ADV-2023-010820-gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/0aa8013eb7eb/BLOODA_ADV-2023-010820-gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/5099bf5ee67c/BLOODA_ADV-2023-010820-gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/de38c72db73c/BLOODA_ADV-2023-010820-gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/609b/11131086/2618b8a13375/BLOODA_ADV-2023-010820-gr6.jpg

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