ArticleSpringerPlus2013
Carbamoylation correlates of cyanate neuropathy and cyanide poisoning: relevance to the biomarkers of cassava cyanogenesis and motor system toxicity.
Article in SpringerPlus, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Glutathione peroxidase 3 is a potential biomarker for konzo.Nature communications · 2024Article
- Review
- Motor control and cognition deficits associated with protein carbamoylation in food (cassava) cyanogenic poisoning: Neurodegeneration and genomic perspectives.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021Article
- Konzo: a distinct neurological disease associated with food (cassava) cyanogenic poisoning.Brain research bulletin · 2019Review
- Cyanide and the human brain: perspectives from a model of food (cassava) poisoning.Annals of the New York Academy of Sciences · 2016Review
- Protein carbamylation in kidney disease: pathogenesis and clinical implications.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2014Review
- Cross-species and tissue variations in cyanide detoxification rates in rodents and non-human primates on protein-restricted diet.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2014Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
We sought to elucidate the protein carbamoylation patterns associated with cyanate neuropathy relative to cyanide poisoning. We hypothesized that under a diet deficient in sulfur amino acids (SAA), the carbamoylation pattern associated with cyanide poisoning is similar to that of cyanate neuropathy. Male rats (6-8 weeks old) were fed a diet with all amino acids (AAA) or 75%-deficiency in SAA and treated with 2.5 mg/kg/body weight (bw) NaCN, or 50 mg/kg/bw NaOCN, or 1 μl/g/bw saline, for up to 6 weeks. Albumin and spinal cord proteins were analyzed using liquid chromatography mass spectrometry (LC-MS/MS). Only NaOCN induced motor deficits with significant levels of carbamoylation. At Day 14, we found a diet-treatment interaction effect on albumin carbamoylation (p = 0.07). At Day 28, no effect was attributed to diet (p = 0.71). Mean number of NaCN-carbamoylated sites on albumin was 47.4% higher relative to vehicle (95% CI:16.7-86.4%). Only NaOCN carbamoylated spinal cord proteins, prominently, under SAA-restricted diet. Proteins targets included myelin basic and proteolipid proteins, neurofilament light and glial fibrillary acidic proteins, and 2', 3' cyclic-nucleotide 3'-phosphodiesterase. Under SAA deficiency, chronic but not acute cyanide toxicity may share biomarkers and pathogenetic similarities with cyanate neuropathy. Prevention of carbamoylation may protect against the neuropathic effects of cyanate.
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Registered trials
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