Bioactivation of cyanide to cyanate in sulfur amino acid deficiency: relevance to neurological disease in humans subsisting on cassava

Tor-Agbidye, John; Palmer, Valerie S.; Lasarev, Michael; Craig, A. Morrie; Blythe, Linda L.; Sabri, Mohammad I.; Spencer, Peter S.

doi:10.1093/toxsci/50.2.228

Cited by 79 publications

(54 citation statements)

References 26 publications

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“…La toxicité directe du cyanure sur les mitochondries ne serait donc possible qu'en cas de saturation des différents systèmes tampons et de détoxification. Le cyanure peut être détoxifié par plusieurs voies, cependant la transformation enzymatique du cyanure en thiocyanate semble être la voie principale [25]. C'est l'enzyme rhodanèse qui est responsable de cette transformation et qui utilise des donneurs de soufre comme cofacteur enzymatique.…”

Section: Discussionunclassified

Une cause rare de neuropathie optique : le manioc

Zéboulon

Vignal-Clermont

Baudouin

et al. 2016

Journal Français d'Ophtalmologie

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Section: Discussionunclassified

Une cause rare de neuropathie optique : le manioc

Zéboulon

Vignal-Clermont

Baudouin

et al. 2016

Journal Français d'Ophtalmologie

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“…This disease is prevalent in populations with dietary deficiency of sulfur amino acids, because of increased conversion of cyanide to cyanate, producing neurotoxicity (318). Cyanate is a proven neurotoxin in experimental studies with animals.…”

Section: Thioretinamide and Sulfate Ester Synthesis From Homocysteinementioning

confidence: 99%

Homocysteine Metabolism, Atherosclerosis, and Diseases of Aging

McCully

2015

Comprehensive Physiology

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The importance of homocysteine in vascular function and arteriosclerosis was discovered by demonstration of arteriosclerotic plaques in children with homocystinuria caused by inherited enzymatic deficiencies of cystathionine synthase, methionine synthase, or methylene-tetrahydrofolate reductase. According to the homocysteine theory of arteriosclerosis, an elevated blood homocysteine level is an important risk factor for atherosclerosis in subjects without these rare enzymatic abnormalities. The homocysteine theory is supported by demonstration of arterial plaques in experimental animals with hyperhomocysteinemia, by discovery of a pathway for conversion of homocysteine thiolactone to sulfate in cell cultures from children with homocystinuria, and by demonstration of growth promotion by homocysteic acid in normal and hypophysectomized animals. Studies with cultured malignant cells revealed abnormal homocysteine thiolactone metabolism, resulting in homocysteinylation of proteins, nucleic acids, and glycosaminoglycans, explaining the abnormal oxidative metabolism, abnormalities of cellular membranes, and altered genetic expression observed in malignancy. Abnormal homocysteine metabolism in malignant cells is attributed to deficiency of thioretinamide, the amide synthesized from retinoic acid and homocysteine thiolactone. Two molecules of thioretinamide combine with cobalamin to form thioretinaco. Based on the molecular structure of thioretinaco, a theory of oxidative phosphorylation was proposed, involving oxidation to a disulfonium derivative by ozone, and binding of oxygen, nicotinamide adenine dinucleotide and phosphate as the active site of adenosine triphosphate synthesis in mitochondria. Obstruction of vasa vasorum by aggregates of microorganisms with homocysteinylated low-density lipoproteins is proposed to cause ischemia of arterial wall and a microabscess of the intima, the vulnerable atherosclerotic plaque.

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“…This state may cause a reduction of rhodanese activity. Under such conditions, hydrogen cyanide is not metabolized to nontoxic thiocyanate, but converted to toxic cyanate (OCN -), which is known to cause neurodegenerative diseases in humans and animals [43].…”

Section: Separation Columnmentioning

confidence: 99%

Mushroom toxins: a forensic toxicological review

et al. 2011

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Mushrooms are ubiquitous in the world. Amateur hunters harvest mushrooms growing in forests to enjoy eating them as seasonal delicacies, and occasionally they cause poisonings and even deaths. In this review, mushroom toxins are tabulated according to mushroom species, symptoms, toxicities and analytical methods on the basis of references. Second, because we constructed a method for analysis of amatoxins, the most virulent mushroom toxins, by liquid chromatography-time-of-flight-mass spectrometry, we introduce it for use in forensic toxicology. Third, an extensive poisoning incident after consumption of the usually edible mushroom Pleurocybella porrigens took place in nine prefectures in Japan from September to December 2004, resulting in 59 poisoned people including 19 deaths; this incident is briefly described and discussed in relation to its causative toxin(s). Finally, we present the chemical structures of new toxins purified from the highly toxic mushrooms Podostroma cornu-damae and Russula subnigricans; their structures were very unique, and the toxicities were comparable to those of amatoxins. From the forensic toxicological point of view, reports on sophisticated methodology for analyses of mushroom toxins seem to be too scant even for the well-known toxins. Hereafter, a number of toxic mushrooms and their new toxins are expected to be disclosed, especially because of environmental changes such as the global warming phenomenon.

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Bioactivation of cyanide to cyanate in sulfur amino acid deficiency: relevance to neurological disease in humans subsisting on cassava

Cited by 79 publications

References 26 publications

Une cause rare de neuropathie optique : le manioc

Une cause rare de neuropathie optique : le manioc

Homocysteine Metabolism, Atherosclerosis, and Diseases of Aging

Mushroom toxins: a forensic toxicological review

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