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Sars-Cov2 Induced Biochemical Mechanisms in Liver Damage and Intestinal Lesions
Liudmila V Spirina1,2, Vladimir N Masunov1, Denis A Dyakov1
1Siberian State Medical University, Tomsk, Russia.
Abstract:
Multiple pathogenic mechanisms are found in SARS-CoV2 systemic inflammation. Oxidative stress, altered proteolysis, hypercoagulation, and metabolic disorders are significant in virus-induced lesions. The study aimed to investigate the biochemical mechanism of virus-induced disorders and determine the biochemical features in SARS-CoV2-associated liver damage and intestine lesions. A retrospective case series of ninety-two patients diagnosed with COVID-19 pnemonia. The ACE, α1-proteinase inhibitor, trypsin-like proteinase, and elastase activity were measured. Nitrites level was detected in reaction with Griess reagent. The ELISA kit measured Troponin, C-peptide, leptin, adiponectin, PAR4, and neuropilin level. It was obtained an increase in ACE activity and nitrites ions content in SARS-CoV2 associated patients. The hyperglycemia and an increase in adipose tissue-derived hormones guided the virus-induced metabolic disorders. Proteolysis activation was revealed in SARS-CoV2 pneumonia patients. The found molecular event was accompanied by hyperglycemia induction. Multiorgan lesions manifest in in cardiac failure, which was detected in patients with ARDS. Moreover, high arterial blood pressure in patients with COVID-19 was associated with the hyperglycemia and increased ACE activity and NO ions level. Liver damage was specific for COVID-19-associated patients with severe ARDS and heart failure. Proteolysis overactivation resulting in vasoactive substances imbalance was detected in patients with the intestinal lesions. The obtained data shows the the neuropilin-dependent axis in damage prevalence in the intestine. Metabolic disorders resulting in the growth of adipose-derived tissue hormones, nitrites, and neuropilin levels was triggered by prolonged inflammation. So, the impaired metabolism and SARS-CoV2 associated hyperglycemia influence on SARS-CoV2 multiple mechanisms. Gastrointestinal manifestations in SARS-CoV2 infection was found to be related to various biochemical and molecular tools. ACE2 receptors axis is prevalent for liver damage, but NRP-1 protein (neuropilin), NO derivatives, and adipose tissue-derived hormones are essential for intestinal lesions.
Supplementary Information:
The online version contains supplementary material available at 10.1007/s12291-022-01089-x.
Insights
COVID-19 causes systemic inflammation through metabolic disorders and proteolysis activation. This study reveals key biochemical markers like ACE, nitrites, and neuropilin involved in liver and intestinal damage, impacting patient outcomes.
Area of Science:
- Biochemistry
- Pathophysiology
- Molecular Biology
Background:
- SARS-CoV-2 infection triggers systemic inflammation with diverse pathogenic mechanisms.
- Oxidative stress, proteolysis, hypercoagulation, and metabolic disorders are implicated in COVID-19 pathogenesis.
- Understanding the biochemical basis of virus-induced organ damage is crucial.
Purpose of the Study:
- To investigate the biochemical mechanisms underlying SARS-CoV-2-induced disorders.
- To identify biochemical features associated with liver and intestinal lesions in COVID-19 patients.
- To explore the role of specific molecular pathways in multi-organ damage.
Main Methods:
- Retrospective case series of 92 COVID-19 pneumonia patients.
- Assay of Angiotensin-Converting Enzyme (ACE) activity, protease activity (trypsin-like, elastase), and α1-proteinase inhibitor.
- Measurement of nitrites, Troponin, C-peptide, leptin, adiponectin, PAR4, and neuropilin levels using ELISA and Griess reagent.
Main Results:
- Increased ACE activity, nitrites, and hyperglycemia observed in SARS-CoV-2 patients.
- Evidence of proteolysis activation and elevated adipose tissue-derived hormones, indicating metabolic dysfunction.
- Liver damage correlated with severe ARDS and heart failure; intestinal lesions linked to neuropilin-1 (NRP-1), nitric oxide (NO) derivatives, and adipokines.
Conclusions:
- SARS-CoV-2 infection induces metabolic disorders and proteolysis, contributing to multi-organ damage.
- ACE2 receptor axis is key for liver damage, while NRP-1, NO, and adipokines are critical for intestinal lesions.
- Impaired metabolism and hyperglycemia significantly influence SARS-CoV-2 pathogenesis and gastrointestinal manifestations.
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