The effect of carbon disulphide on the metabolism of pyridine nucleotides and nicotinamide.

Details

• Personal Author:
  Wronska-Nofer T
• Description:
  The toxic action of carbon disulphide is many sided. For example, it has been known, that, depending on the severity of exposure, the prevailing symptoms may be the result of a neurotoxic action (at higher concentrations) or a vasculotropic one (at lower concentrations). Similarly, various known biochemical disturbances in the organism may be caused by this compound. At present, it seems difficult to answer the question whether the different disturbances appear independently each from the other or as a center of initial action with derivative symptoms which are being actually observed. Our present studies on the metabolism of nicotinic acid in the course of carbon disulphide intoxications were started on the basis of the following earlier observations: 1. Exposure to CS2 brings about disturbances in the urinary level of the nicotinic acid, manifested by an increase of the N1-methylnicotinamide. That was first observed by Liniecki and later confirmed by Wrorfska et al. to occur in rats. However, similar disturbances were also found in workers exposed to CS2, in the viscose rayon industry. Moreover, some quantitative relationship was observed between the elevation of N1-methylnicotinamide and the actual concentration of CS2 in the air (Fig. 1). It was found in rats exposed to a concentration of 0.9 mg/l of CS2 that increase of N1-methylnicotinamide in the urine takes place already at the beginning of chronic exposure (after 2 days), reaching a steady state of the elevated level after one week of exposure (Figure 2). 2. Some biological importance of the above disturbances seem evident if one considers the influence of nicotinic acid on the pathways of the lipid metabolism: Chronic exposure to CS2 results in changes of the lipid metabolism consisting of an increase of the cholesterol, phospholipids and triglycerides in blood. These changes could be prevented by feeding of the animals with nicotinic acid. The biochemical background of the above phenomenon is still obscure. With respect to the changes in the metabolism of nicotinic acid it seemed to be interesting to find out the sources of the excess of nicotinic acid appearing in the urine in form of the N1-methylnicotinamide, if constant uptake of nicotinic acid from the food is accepted. The existing data point to the fact that the bulk of the systemic nicotinamide is present in the body in the form of nicotinamide adenine nucleotides. Therefore, theoretically at least, the only source for the elevated levels of nicotinic acid could be the ·pool of the nucleotides; carbon disulphide could, eventually, increase their degradation rate, resulting in an increased excretion of the nicotinamide (as a methylated derivative or nicotinic acid). If this hypothesis is taken as a basis, two possibilities seem to have existed: (a) the increased degradation rate of nucleotides has been accompanied by similar increase in the rate of synthesis (increased total turn over rate), allowing the actual absolute level of nucleotides to remain unchanged; (b) otherwise, when there was no increase in the synthesis of nucleotides, the elevated excretion would result in a depletion of the systemic levels of the nucleotides if the exposure to CS2 had persisted for a sufficiently long time. In the present studies attempts were undertaken to answer the following questions: a. Whether, apart from disturbance of N1-methylnicotinamide, also the excretion of other metabolites of nicotinic acid is disturbed by exposure to CS2; b. Whether the elevated excretion of the nicotinic acid metabolites is reflected by a drop in the level of systemic nucleotides, and c. What is the biochemical background of the disturbances in question. Attempts to approach the above problems are given below in detail.
• Subjects:
  Accidents, Occupational Economics Fatigue Mental Health Nervous System Occupational Health Safety Shift Work Schedule Sleep Stress, Psychological
• Keywords:
  Biochemical Effects Carbon Disulfide Chronic Exposure Exposure Assessment Health Effects Metabolic Effects Metabolites Nucleotides Occupational Exposure
• Publisher:
  National Institute for Occupational Safety and Health
• Document Type:
  Text
• Funding:
  Grant
• Genre:
  Conference/Symposia Proceedings
• Place as Subject:
  Ohio ; OSHA Region 5
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Pages in Document:
  63-92
• NIOSHTIC Number:
  nn:20057366
• Citation:
  Proceedings of the Special Foreign Currency Program Symposium, October 1970, Dubrovnik, Yugoslavia. Henschel A ed. Cincinnati, OH: U.S. Department of Health, Education, and Welfare, Public Health Service, Health Services and Mental Health Administration, National Institute for Occupational Safety and Health, 1970 Oct; :63-92
• CAS Registry Number:
  Carbon disulfide (CAS RN 75-15-0)
• Editor(s):
  Henschel A
• Federal Fiscal Year:
  1971
• Peer Reviewed:
  False
• Source Full Name:
  Proceedings of the Special Foreign Currency Program Symposium, October 1970, Dubrovnik, Yugoslavia
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:31a8775326f01bffbee4073c5cd03e5363f7ab76e266fb68738414f054ff05cb69c95d386528546424cebfbdac5b0f628455af752c0a80d39330f207c75f6ac7
• Download URL:
  https://stacks.cdc.gov/view/cdc/181815/cdc_181815_DS1.pdf
• File Type:
  [PDF - 3.68 MB ]