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瑞士韦伯斯特小鼠中毒的时间进程病理生理学:对全身表现的见解

Time-Course physiopathology of Envenomation in Swiss Webster Mice: Insights into Systemic Manifestations.

作者信息

Montealegre-Sánchez Leonel, Lima Mikael A, Montoya-Gómez Alejandro, Solano-Redondo Luis, Silva Dayara O, Alves Pereira Karuza M, Lima Mota Mario R, Silveira Edilberto Rocha, de Sousa Brasil Nilce Viana Gramosa Pompeu, Alves Filho Elenilson G, Havt Alexandre, Jiménez-Charris Eliécer

机构信息

Grupo de Nutrición, Facultad de Salud, Universidad del Valle, Cali, Colombia.

Grupo de investigaciones en Ingeniería Biomédica-GBIO, Facultad de Ingeniería, Universidad Autónoma de Occidente, Cali, Colombia.

出版信息

Sci Prog. 2025 Jan-Mar;108(1):368504241304205. doi: 10.1177/00368504241304205.

DOI:10.1177/00368504241304205
PMID:39763189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11705321/
Abstract

OBJECTIVE

The expansion of human activities in northern Colombia has increased human-snake encounters, particularly with venomous . Given the limited knowledge of systemic envenomation effects and previous studies focusing only on early murine symptoms, this investigation aimed to describe the time-course physiopathology of envenomation following intramuscular injection .

METHODS

Venom was inoculated in the gastrocnemius muscles of Swiss Webster mice, and blood, urine, and tissue samples were taken at different times to evaluate lethality and biochemical markers of renal function and oxidative stress.

RESULTS

This study reports the first intramuscular LD for venom at 24.83 mg/Kg. Administering 80% of this LD induced early signs of renal injury, evidenced by urinary biomarkers over 24 h. The antioxidant activity was found at low levels in kidney tissue throughout the evaluated time post-envenomation. Malondialdehyde activity increased at the earliest point, while proinflammatory activity increased later. Urine metabolomics revealed elevated taurine and allantoin in the envenomed groups.

DISCUSSION

Compensatory mechanisms in response to oxidative stress and tissue damage induced by the venom were evident in the envenomed mice over the evaluated time. However, histological analysis revealed evidence of pro-inflammatory processes occurring only at early times. Metabolomic analyses of urine samples identified taurine as a potential early biomarker of elevated oxidative stress and protein and creatinine levels.

CONCLUSIONS

venom induces alterations in murine renal tissue, affecting urinary biomarkers of kidney function within hours post-envenomation. Delayed proinflammatory effects may suggest an antioxidant imbalance in the envenomed mice, with unknown long-term effects. Further research on the role of oxidative stress and inflammation in renal structure and function following envenomation is necessary, emphasizing the need for prompt clinical management.

摘要

目的

哥伦比亚北部人类活动的扩展增加了人类与蛇的接触,尤其是与有毒蛇类的接触。鉴于对全身中毒效应的了解有限,且以往研究仅关注早期小鼠症状,本研究旨在描述肌肉注射后中毒的时间进程生理病理学。

方法

将毒液接种于瑞士韦伯斯特小鼠的腓肠肌,在不同时间采集血液、尿液和组织样本,以评估致死率以及肾功能和氧化应激的生化标志物。

结果

本研究报告了该毒液的首次肌肉注射半数致死量为24.83mg/Kg。给予该半数致死量的80%可诱导肾脏损伤的早期迹象,24小时内尿液生物标志物可证明这一点。在中毒后的整个评估时间内,肾脏组织中的抗氧化活性处于低水平。丙二醛活性最早升高,而促炎活性随后升高。尿液代谢组学显示中毒组中牛磺酸和尿囊素升高。

讨论

在评估时间内,中毒小鼠对毒液诱导的氧化应激和组织损伤的代偿机制明显。然而,组织学分析显示仅在早期有促炎过程的证据。尿液样本的代谢组学分析确定牛磺酸是氧化应激升高以及蛋白质和肌酐水平升高的潜在早期生物标志物。

结论

该毒液可诱导小鼠肾脏组织发生改变,在中毒后数小时内影响肾功能的尿液生物标志物。延迟的促炎效应可能表明中毒小鼠存在抗氧化失衡,长期影响未知。有必要进一步研究氧化应激和炎症在中毒后肾脏结构和功能中的作用,强调及时临床处理的必要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/a5727fa9b144/10.1177_00368504241304205-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/d0599fc06834/10.1177_00368504241304205-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/29e29ec7b0e9/10.1177_00368504241304205-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/7615d2406549/10.1177_00368504241304205-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/93d238f2d413/10.1177_00368504241304205-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/f2762855d517/10.1177_00368504241304205-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/a5727fa9b144/10.1177_00368504241304205-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/d0599fc06834/10.1177_00368504241304205-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/29e29ec7b0e9/10.1177_00368504241304205-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/7615d2406549/10.1177_00368504241304205-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/93d238f2d413/10.1177_00368504241304205-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/f2762855d517/10.1177_00368504241304205-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6866/11705321/a5727fa9b144/10.1177_00368504241304205-fig6.jpg

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