S Balabaskaran

The effect of soy protein on the small bowel mucosa of 18 infants with acute gastroenteritis was studied. The infants were maintained on a protein hydro-lysate formula for 6–8 weeks, following which they were readmitted for soy protein challenge studies. Jejunal biopsy was performed before and 24 h after challenge. On the basis of the clinical and histological reaction to soy protein challenge, three groups were identified. Group 1 consisted of three infants who had clinical and histological reaction. There was associated depletion of mucosal enzymes, lactase, sucrase, malatase, alkaline phosphatase, and blood xylose levels. Group 2 consisted of seven infants who had histological reaction but no clinical symptoms. Two of these seven infants, however, developed clinical reaction when rechallenged with soy protein 2 and 90 days later. Following challenge, mucosal enzymes and blood xylose levels were depressed in five of the seven infants tested. Group 3 consisted of eight infants who did not have either a clinical or a histological reaction. The mucosal enzymes and blood xylose levels were not depressed in four infants tested. The present study shows that the small bowel mucosa of some young infants recovering from acute gastroenteritis remains sensitive to soy protein for a variable period of time. The feeding of soy protein to these infants may result in the persistence of mucosal damage and perpetuation of diarrhea. These findings have an important bearing in the nutritional management of infants recovering from AGE; the exclusion of soy protein from the diet of these infants, particularly during the period when the mucosa is damaged, may reduce the risk of the development of soy protein sensitive enteropathy and the attendant complication of protracted diarrhea.

Abstract Structure–activity relationship studies were conducted with early fourth‐instar larvae of a highly resistant strain of the diamondback moth, Plutella xylostella (Linnaeus) on (1) toxicity by topical appliction of 43 organotin compounds, and (2) the antifeedant effect of a selected number (17) of these compounds on treated Brassica chinensis (Chinese cabbage) leaves. The toxicity data revealed that the triorganotins (R 3 SnX) were, without exception, more toxic than the commercial sample of malathion (84% active ingredient) used in the tests. Among the diorganotins, phenylcyclopentyltin oxide proved to be as active as malathion. Within the triorganotin series, the tricyclohexyltins were generally more toxic than the triphenyltins, the most active tricyclohexyltin compound being (c‐C 6 H 11 ) 3 Sn(2‐pyridinethiolato N ‐oxide) (LC 50 0.03 μg μl −1 ), which was almost 500‐fold more active than malathion. The most active compound in the triphenyltin class was O, S ‐bis(triphenyltin)mercaptoacetate (LC 50 0.30 μg μl −1 ). Variations in the anionic X group resulted only in marginal changes in activity in the (c‐C 6 H 11 ) 3 Sn series, but significant changes in activity were obtained with the Ph 3 Sn compounds, especially the ring‐substituted phenoxyacetates, (4‐ZC 6 H 4 )OCH 2 (O)COSnPh 3 . In the mixed triorganotin compounds an increase in activity was observed when one of the phenyl groups in Ph 3 SnOH was replaced by the p ‐chlorophenyl group. In the antifeedant tests, the tricyclohexyltins were found to be generally more effective than the triphenyltins. In most cases, antifeedant activity paralleled the toxicity by topical application trends in the (c‐C 6 H 11 ) 3 Sn series, but in the Ph 3 Sn series an inverse trend was observed. The diorganotin compound (c‐C 5 H 9 )PhSnO exerted a relatively pronounced antifeedant activity which was comparable with that of a number of triphenyltin derivatives. It was established from histological studies of the mid‐gut cross‐sections of the treated larvae that, in most cases, the organotins affected the columnar cells physiologically; an exception was noted for Ph 3 SnOC(O)C 6 H 4 COOH‐4 which, like malathion, caused severe morphological damage to the cell membrane.

Triphenyltin coumarin-3-carboxylate and its coordination complexes with ethanol, triphenylphosphine oxide, triphenylarsine oxide, diphenylcyclopropenone and quinoline N-oxide exhibited high in vitro cytotoxicity (LC(50) values in the range 0.25-3.4 mug/mL) when tested against EBV-DNA positive Raji cells and P-388 leukaemia cells, compared to the standard drug 5-Fluorouracil, which showed LC(50) values of 11 and >50 mug/mL, respectively, against these cells. Additional tests performed on the Raji cells incubated with the quinoline N-oxide complex in the presence of the tumour promoters, TPA and sodium butyrate, revealed that the diffused and restricted protein components of the early antigen complex were suppressed relative to the control containing only the promoters, indicating impaired function of the genes involved as transactivators in the early lytic cycle of the EBV. The failure of the restriction enzymes Eco R1 and Hind III to cleave the extracted DNA from such treated cells in contrast to the control, coupled with the amplification of the BMLF-1 gene by the PCR technique which was realised only with the DNA of the control and not of the treated sample, point to a punitive interaction of the organotin with the nuclear DNA of the Raji cells.