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Medicine with Deeper, More Biochemical Conception Of Edinburgh Medical Journal May 1951 APPLICATIONS of chemical defence research IN MEDICINET? By Professor R. A. PETERS to be invited It is a great responsibility, as well as a great honour, to Cameron lecturers give this lecture ; and I expect that with other I this ancient seat of share a sense of awe upon standing here in is learning. For me it is an awe tinged with much feeling (it possible that this is partly because some forebears of my mother came from near to recent of the this ; it is in part due the perusal city) perhaps " address here Froude in on the Times of John Knox, given by 1865 " " entitled Influence of the Reformation upon the Scottish Character ; this address drives home to the Sassenach the sterner stuff of which all of us in the the Scots are made ; but I really think it is more that as south, even if we come as I do from a Medical School as ancient the Hospital of St Bartholomew, know full well that Edinburgh stands high indeed in the world of Medical Schools as Scotland itself stands in the world of intellect. Elsewhere I have discussed fully the historical background of our for me back researches upon Chemical Defence substances, which go to World War I.23 Again in my Dixon lecture,24 I have indicated some of the interest for pharmacology. The outlook for medicine has not the been reviewed so far. Therefore I propose to-day to discuss of British influence upon the future of therapeutics of the discovery anti-lewisite and of some of the other researches upon war gas but substances ; and to consider not only the leads towards therapy, the possible newer trends given to medicine itself. touch The Chemical Warfare substances upon which I shall to-day are the arsenicals and British anti-lewisite, the mustard gases, diiso- the propyl fluorophosphonate (DFP) and finally fluoroacetate. With researched exception of DFP, at some time or other, I have personally been done in upon all the others, and in the case of DFP, work has crew so far my laboratory by others.32 The substances are a motley as In order to their chemistry is concerned, and somewhat unruly. to a review allow time for some generalisation, I must confine myself ?f those who have a the main points concerned ; and I hope that Cameron Prize Lecture delivered 6th November 1950. some of these are This lecture was illustrated by lantern slides ; only reproduced here. o VOL. LVIII. NO. 5 198 R. A. PETERS specialised interest in any of them will excuse a presentation which to them must appear somewhat incomplete. It should be made clear at the outset that I feel I stand here as the leader and spokesman of a splendid group of colleagues who took part in these researches in my laboratory during the last war in Oxford ; with the British anti-lewisite investigation must be mentioned especially L. A. Stocken and R. H. S. Thompson,30 and with that on mustard gas A. G. Ogston and J. St L. Philpot; several others played a significant role. It is convenient to start from the experimental development of the idea that we must look for the origins of pathological change in alterations of the biochemistry of tissue cells. In order to make this idea concrete, I introduced the term "biochemical lesion" in 1931 when working with Gavrilescu, to indicate that there was an initial biochemical change preceding any pathological changes. As a result of an analysis of the condition of opisthotonus induced by vitamin Bx deficiency in the pigeon, we were able in my laboratory to state categorically that this pathological condition is due to lack of the co- enzyme for the pyruvate oxidase system in the tissue of the brain ; that is to say, it is concerned with an intermediate stage in the meta- bolism of sugar. As I thought, this proof when taken together with other work means no less than this ; a new era was dawning for medicine with a deeper, more biochemical conception of pathological change. This is why I feel that I am speaking now also for biochemists in general in so far as I am stressing a biochemical view of disease ; it formed the background to our war research, and in its development several colleagues have helped me substantially during the last twenty years, including Dr A. P. Meiklejohn and Dr R. Passmore, who are now ir this University. " In 1936, I ventured to write in the Lancet as follows 21: We are so accustomed to the detailed analysis upon the fixed tissue which is made possible by refined histological methods that we do not readily adjust to the idea that a new type of analysis is being steadily perfected by modern biochemical research ; we can obtain information of changes too subtle to be recorded upon the fixed histological specimen, changes in the behaviour of essential enzyme systems present." This point of view is now rather clear to most biochemists ; but I do not think that medicine as a whole has become adapted even yet to the realisation that in the histological specimen we are looking at the end result of a biochemical disturbance, and that it would have been better for a therapeutic effect if we could have detected the enzyme abnormalities before they had become sufficiently advanced to disorganise the tissue. Admittedly it was somewhat of a revolution, though the ideas are in essence simple.* * Of course no one would suggest that the older empirical method should be discarded. It is a matter of addition. CHEMICAL DEFENCE RESEARCH IN MEDICINE 199 I have referred to this old work here not only because it played a significant part in the war developments ; but because, particularly, I want to show how the rather diverse researches in this chemical defence field have all centred upon tissue biochemistry. It is relevant to say that when our war work started twelve years ago, there was wide scepticism, ranging from circles of pure chemistry to those of act tissue medicine, as to whether toxic substances could upon living this was in of the evidence by an initial attack upon cell enzymes ; spite in then available on the nature of the biochemical lesion vitamin B2 deficiency, and also of the implications of the important work on choline esterase in which Edinburgh University played so important a part.29 Fructose 6>osphate Fructose 1:6 diphosphate Dihydroxijacetone' phosphate Glucose 6t , phosphate' f? I' (2)QIyceraldenaepnosp(iduchaephosphate Glucose 1*I phosphatenhosnhate \inosepnuiHuoL\Triosephosphate dehydrogenase] <IODOACETATE 4 (2) 1:3 Diphosphoglijcerate en Glycog (2) 3: Phosphogkjcerate (2) 2: Phosphoglycerate \ (Z) 2: Phosphopyruvate sasfA Further products time. Fig. 1 asas conceived atat the the I.?Shows??Shows the the course course of of degradation degradation of of carbohydrate carbohydrate conceived present shows the course of EachEach step step is is catalysed catalysed by by a a distinct distinct enzyme. enzyme. ThoughThough the the diagram diagram conditions.conditions. It will^ be sgen seen that that degradation,degradation, all all the the stages stages are are reversible reversible under under suitable suitable oxidation. arsenicalsarsenicals make make a aprimary primary attack attack upon upon pyruvate pyruvate oxidation. remarks Arsenicals and British Anti-Lewisite.?It will orient my taken at the modern upon the arsenicals better if a cursory glance is view It will be noted of the course of degradation of carbohydrates. series of that deficiency of vitamin acts at the same point in this on the initial of phosphoester reactions as arsenicals, namely stage Pyruvate oxidation (Fig. i). last war I started work within two days of the beginning of the was this upon the hypothesis that the most sensitive enzyme pyruvate in a vulnerable ?SH oxidase system and that this was attacked 200 R. A. PETERS (sulphydril) grouping upon one of the proteins, an ?SH group that is essential for the functioning of the enzyme-system. These postulates were a logical inference partly from work in my laboratory and partly from work elsewhere ; the roots of this in both cases went back many years. Confirmation of the selective action of arsenicals on the pyruvate system was soon obtained. Support for sensitivity of pyruvate oxidation to arsenicals was further found in vivo in the fact shown in TABLE I Effect of Injected Arsenite on the Blood-Pyruvate Level of Pigeons Pyruvate, determined by 2 : 4-dinitrophenylhydrazone Method. (Mg. Pyruvic Acid/100 g. Blood.) Total Dose (mg. As,Oj). Normal. Acute. Chronic. 1-28 4-02 (2 hrs.) 12-39 ( 4 days) 8-5 o-94 3-oo (2 ? ) 14-15 (4?) 8-5 ?'94 3-12 (2 ? ) 13-85 (43 ? ) 7-0 6-30 (3 ? ) Mean 1*06 4-n 13-47 (From data of Peters, Sinclair and Thompson, 1946) Note.?Similar results were obtained using the bisulphite binding method, and with the arsenical lewisite. Table I that these poisons led to an increase of pyruvate in the blood, similar to that found in vitamin Bx deficiency. It was also shown that a sensitive ?SH grouping was present. Turning now to a consideration of British anti-lewisite itself, it may be asked what it is and what it does. British anti-lewisite is a dithiol substance known chemically as 2-3 : dimercaptopropanol (now called dimercaprol). H2C.SH I H C.SH I h2c.oh Of a series of substances of similar constitution, it has turned out to be the least toxic with one exception. A large number of similar dithiol substances were made in the United Kingdom, U.S.A.
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