of both x andchains within the same cell* suggests that it may have been phagocytosed rather than synthesised by these cells. We have observed intracytoplasmic immunoglobulin in Reed-Sternberg cells in sections and in freshly dispersed cell preparations by both the immunofluorescence and the immunoperoxidase technique but never in cells that have been maintained in culture for more than 24 h. Evidence from Curran and Jones and Cossman et al.7 suggests that the small lymphocytes, seen in tissue sections to be associated with Reed-Sternberg cells, are B cells. We have found, however, that most small lymphocytes yielded by dispersion of fresh biopsy material are T cells.s The role of these T cells remains unclear yet they appear to have a specificity for the Reed-Sternberg cells because they will attach themselves to and migrate over the tumour-cell surface when freshly dispersed cells are cultured.4.9A report that these T cells can kill the tumour cell within 30 min in culture10 seems to support the suggestion that this adherence is a manifestation of an immunological response directed against the tumour cells."Our results, however, suggest that these T cells are not cytotoxic since after several days in culture the ReedSternberg cells within cell clusters remain viable despite increased lymphocyte attachment. Furthermore, these clusters may persist for as long as 5 weeks in culture, although by then the number of attached lymphocytes has usually decreased (figs.1 and 2). It is possible that these cell clusters represent an aberrant attempt at cell cooperation12 rather than an immunological attack. S. V. PAYNE University Department of Pathology, D. B. JONES Southampton General Hospital, D. H. WRIGHT Southampton SO9 4XY sence

SALICYLHYDROXAMIC-ACID/GLYCEROLIN EXPERIMENTAL TRYPANOSOMIASIS SIR,—The human and veterinary African trypanosomiases remain diseases of great social and economic importance, and any new drug with action against the causative trypanosomes would be very welcome. We wish to report the trypanocidal activity of a combination of salicylhydroxamic acid (s.H.A.M.), a compound which has been tried as an anti-tuberculosis drug in man,’ and glycerol. S.H.A.M. is a specific inhibitor of the unique cyanide-insensitive respiration of the African sleeping-sickness trypanosomes (Trypanosoma brucei group )2.3 and of T. vivax4 which causes a fatal disease in domestic cattle and sheep. On its own, S.H.A.M. is ineffective as a trypanocide in vivo, but when combined with glycerol it temporarily clears bloodstream trypanosomes in rodents infected with T. brucei.5 The cure was, however, never complete, and trypanosomes always reappeared in the blood within seven days. We have shown that mice inoculated with recently isolated strains of T. brucei rhodesiense and T. brucei brucei and treated with S.H.A.M. (430 mg/kg) and glycerol (36 g/kg) one day after inoculation have remained aparasita:mic for three months, while control animals die within three weeks with 6

Taylor, C.R. Eur. J. Cancer, 1976, 12, 61. 7 Cossman, J , Deegan, M. J., Schnitzer, B.Cancer, 1977, 39, 2166. 8 Payne, S. V., Jones, D.B., Haegert, D. G., Smith, J. L., Wright, D. H. Clin. exp Immun. 1976, 24, 280. 9 Pulvertaft, R. J. V. Proc. R. Soc. Med. 1959, 52, 315. 10 Kay,M M B. Rec. Results Cancer Res. 1976, 56, 111. 11 Archibald, R. B., Frenster, J. H. Natn. Cancer Inst. Monog. 1973, 36, 239. 12 Stuart, A. E., Williams, A. R. W., Habeshaw, J. A. J. Path. 1977, 122, 81. 1 Urbanski, T. Nature, 1950, 166, 267. 2 Evans, D. A., Brown, R. C. Trans. R. Soc. trop. Med. Hyg. 1973, 67, 258. 3 Opperdoes, F. R., Aarsen, P. N., Vam Den Meer, C., Borst, P. Expl. Parasit.

1976, 40, 198. 4 5

Vickerman, K., Evans, D. A. Trans. R. Soc. Trop. Med. Hyg. 1974, 68, 145. Clarkson, A. B., Brohn, F. H. Science, 1976, 194, 204.

overwhelming parasitæmia. If, however, the treatment was delayed until the parasitxniia was patent in the peripheral blood (approximately one week post-inoculation), then permanent cures were not affected by this treatment. With patent T. vivax infections of different durations, the above treatment with S.H.A.M. and glycerol has always resulted in radical cures, the animals remaining clear of trypanosomes so far for two months. The difference in the curative effect of S.H.A.M. and glycerol is thought to be related to differences in the distribution of the organisms in the body of the host: T. vivax is confined to the blood-vessels whereas T. brucei is distributed more widely in both blood and tissue fluids. D. A. EVANS C. J. BRIGHTMAN*

Department of Medical Protozoology, London School of Hygiene and Tropical Medicine,

M. F.

London WC1E 7HT *Present address. London NW 10.

Department

of

Microbiology,

HOLLAND

Central Middlesex

Hospital,

LABORATORY CONTAMINATION BY RADIOACTIVE IODINE

SIR,—Unexpected hazards may arise in the handling of compounds labelled with radioactive iodine.’-3 Iodine atoms which are covalently bonded to labelled molecules can be released into solution as iodide ions. These are oxidised to iodine molecules whose low solubility causes their release into the atmosphere. This upsets the solution equilibrium between iodide ions and molecular iodine, and the result can be substantial loss of radioactive iodine from solution to the atmosphere with the consequent risk of its inlialation. We have seen an example of contamination arising from the use of 125I in a laboratory doing radioimmunoassays. Nearly all surfaces in the laboratory were contaminated. The incident demonstrates the usefulness of routine wipe testing. The laboratory had been using 121-labelled protein for routine radioimmunoassay for two months; the laboratory had not previously worked with radioactive substances. The 1251 solutions were of specific activity up to 10 µCi/ml, and total usage did not exceed 3 mCi per month. The volume of the laboratory was approximately 480 m3. Several workers used 125I.in different parts of the laboratory and the total activity of material in use at any one time was several tens of microcuries. Wipe tests had been taken routinely over the two months. Wipes were taken over 1000 cm2 and counted in a Y wellcounter of approximately 20% efficiency. A removal factor of 10% was assumed. A wipe giving 7500 counts in 100 s represented surface contamination of 0.1nCi/cm2. The background was 30-40 counts in 100 s. The procedure could, therefore, detect contamination down to approximately 1 pCi/cm2. In contrast the sensitivity of direct monitoring4 for 125I is at best only 0.nCi/cm2. Over the first two months there were no reports of excessive contamination on working surfaces. These surfaces-were regularly cleaned. After two months of work with radioactivity wipes were then taken on surfaces such as floors, walls, ceilings, and cupboards which were not cleaned as regularly or thoroughly. Surprisingly these surfaces gave gross counts representing uniform contamination throughout the room of the order 3 pCi/cm2. y spectrometry confirmed that the nuclide responsible was 125I. There was no evidence of air contamination at this time, and no contamination was detected in neighbouring rooms or corridors. The total 125I on surfaces throughout the laboratory was estimated as 20 µCi. The 1. Bogdanove, E. M., Strash, A. M. Nature, 1975, 257, 426. 2. Howard, B. J. J. nucl. Mea. Technol. 1976, 4, 28. 3. Lancet, 1976,i, 133. 4. Linsley, G. S. Criteria for Safe Working with I-125. National Protection Board, 1976.

Radiological

770 remarkable feature was the uniformity of the contamination: clearly the activity has been deposited from the air. All surfaces were decontaminated. The fan in the fume cupboard of the laboratory had been out of operation over the two-month period. Subsequently as many operations as possible were done in the fume cupboard, even though it would not normally be considered necessary to work in a fume cupboard at the activities involved. The fan was run continuously to promote air changes. Over the next three months no surface contamination was detected, except on working surfaces.

positive for HBeAg and 45.5% are positive for HBeAb. Owing to vagaries of the immune response and the sensitivity of the techniques used, it is not clear whether the remaining 50% have been exposed to e antigen.

Radiochemical Laboratory, Department of Chemistry, University of Dundee, Dundee DD1 4HN

Department of Medical Microbiology, University College,

I. S. MCLINTOCK

Department of Obstetrics and Gynæcology, University of Dundee

J.

We thank Dr J. Wallace, of the Glasgow and West of Scotland Regional Transfusion Centre, for his help. This work was supported by a grant from the Distillers Company Limited.

University Department Royal Infirmary, Glasgow, G4 0SF

M. J. PARKER R. B. GOUDIE A. G. SHATTOCK

Belfield, Dublin

L. YOUNG

DISULFIRAM-INDUCED MYOCARDIAL AND SKELETAL-MUSCLE DEGENERATION IN RATS

CEREBRAL BLOOD-FLOW IN POLYCYTHÆMIA

SIR,—The paper by Dr Thomas and his colleagues (July 23, 161) may be relevant to patients with hypoxic lung disease and secondary polycythsemia. Such patients frequently have cerebral symptoms which are usually attributed to the low

p.

. p a02 and raised Paco2. After isovolumetric venesection (e.g., with dextran 40) there is usually a clinical improvement in these symptoms but no concomitant change in blood gases or respiratory-function tests.’ When the packed cell volume rises the benefits of increased oxygen carriage are outweighed by the exponential increase in blood viscosity and the resultant reduction in blood-flow.2 It is unlikely that altered renal perfusion plays a role in this improvement-indeed venesection should probably be done only on patients with a normal blood-urea.3 Much of the apparently subjective improvement reported by patients with polycythaemic chronic obstructive lung disease after isovolumetric venesection may result from increased cerebral blood-flow. Brook General London SE18

of Pathology,

Hospital, DAVID HONEYBOURNE

SIR,-Disulfiram has been used as a fungicide and rubber chemical and for the treatment of alcoholism. Like many other thiocarbamates it is biotransformed to carbon disulphide.1,2 Many of the toxicological properties of disulfiram, such as its neurotoxicity, may be attributed to this biotransformation product. Animal studies on carbon disulphide,3,4 disulfiram,s and thiram6 have described muscle incoordination, ataxia, and tremor as well as paralysis, suggesting that the neurotoxic effects of carbon disulphide may lead to muscle impairment. We have looked for morphological effects of disulfiram on skeletal muscle and myocardium. 30 Sprague-Dawley rats of each sex were given disulfiram

120, mg/kg body-weight daily by

gavage

as a

microsuspension

in ’Methocel 65 Hg’ water solution. The same number of control animals were given the vehicle alone. Five animals of each

1. Johnston, C. D., Prickett, C. S. Biochim. biophys. Acta. 1952, 9, 219. Fischer, R., Brantner, H. ArzneimittelForsch., 1967, 17, 1461. Lewey, F. H. J. ind. Hyg. Toxicol., 1941, 23, 415 Wronska-Nofer, T., Stetkiewicz, J., Szendzikowski, S. Int. Arch. Arbeitsmed. 1973, 31, 123. 5. Child, G. P. Crump, M. Acta pharmac. toxicol., 1952, 8, 305. 6. Lee, C. G., Peters, P. J. Envir. Hlth Perspect. 1976, 17, 35.

2. 3. 4.

INCIDENCE OF HBe ANTIGEN AND HBe ANTIBODY IN BLOOD-DONORS

SIR,-In South-West Scotland 0-2% of healthy blood-

hepatitis-B surface (HBs) antigensemia as assessed by radioimmunoassay. 88 HBsAg-positive plasmas from blooddonors were examined for the presence of e antigen (HBeAg) and anti-e antibody (HBeAb) by an immunodiffusion technique. Several plasmas, mainly high-titre HBeAb-positive, produced multiple lines and for this reason results were considered positive only when they produced a line of confluence with standard HBeAg and HBeAb. All negative samples were concentrated fourfold by ultrafiltration and tested against a panel of e and anti-e positive plasmas. This was found, greatly enhancing the sensitivity of HBeAg detection. The sensitivity ofHBeAb detection was 29% greater: donors have

These findings demonstrate that approximately 50% of HBjAg carriers have evidence of e-antigen exposure: 3-4% are Harrison, B. Gregory, R., Clark, T., Scott, G. Br. med. J. 1971, iv, 713. Dintenfass, L., Read, J. Lancet, 1968, i, 570. 3. Honeybourne, D. Br. med. J. 1977, i, 52.

1. 2.

Fig. 1—Section firam 120

of rat

myocardmm after treatment with disul-

mg/kg/day

for 14

myocardial degeneration. (H. & E.-, x 250.)

days showing acute-subacute