PubMed · 5962738
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T Harada. 1966. [Cholinesterase].. https://pubmed.ncbi.nlm.nih.gov/5962738/
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Many theories have been advanced but the true physiological function for serum cholinesterase has still not been identified. Evidence has been presented for the abnormal expression of cholinesterase genes in many types of human tumors. Cholinesterase measurements are still used to monitor exposure to organophosphate insecticides and their clinical application requires a good understanding of the inter and intra-individual variation, as well as some knowledge of the time sequence between exposure and measurement of the cholinesterase activity. The use of serum cholinesterase measurement in liver disease varies in different countries. A case has not been made for the cost-effectiveness of adding serum cholinesterase as part of a screening procedure for the diagnosis of liver disease. During the last 10 years much information has been obtained on the molecular biology and genetics of acetylcholinesterase and butyrylcholinesterase, distinct enzymes encoded by two different, but related genes. It has been established that BChE is included by a single gene which corresponds to the E1 locus. The complete amino acid sequence of human serum cholinesterase and the location of disulfide bonds within the sequence have been described. The molecular basis of many variants of human serum cholinesterase has been described in detail. It is not rare for multiple mutations to occur within a single butyrylcholinesterase gene or there may be combination of mutations. At least 11 silent variants of human butyrylcholinesterase have been identified. There still exists a wide variety of substrates and analytical conditions for butyrylcholinesterase measurement in a number of clinical situations. No real evidence has been provided for clinical value for their use in the diagnosis of Alzheimer disease or monitoring the use of cholinesterase inhibitors in the treatment of pre-senile dementia of Alzheimer type. However, the insights from molecular biology technology may well open up more challenges in a variety of clinical situations.
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A cross sectional study was conducted in September 1989 in order to estimate the prevalence of organophosphate exposure and to identify factors associated with increased organophosphate exposure in pesticide producing factories in Harare, Zimbabwe. Sixty five workers entered the study with 45 of them providing blood specimens. The mean cholinesterase level was 75.3 pc (standard deviation 21.07 pc). Twenty (44.4 pc) workers had cholinesterase levels of less than 75 pc. The workers had adequate knowledge (75 pc+) of the importance of protective devices but had less knowledge of about 50 pc of health effects of pesticides. Smoking (t = 3.49; degrees of freedom (df) = 43; p < 0.01) and eating (t = 2.14; df = 43; p < 0.05) at work place were associated with increased exposure to organophosphate. The number of symptoms was not correlated with cholinesterase levels (Spearman's rank correlation coefficient--0.70; p = 0.12). We conclude that a significant number of workers were exposed to organophosphate. Increased personal hygiene such as washing hands before eating or smoking should reduce the amount of exposure.