The polyamines putrescine, spermidine and spermine are essential for cell renewal and, therefore, are needed to keep the body healthy. It was previously believed that polyamines are synthesized by every cell in the body when required. However, in the present paper evidence is provided to show that, as in the case of the essential amino acids, the diet can supply sufficient amounts of polyamines to support cell renewal and growth. Systematic analysis of different foods was carried out and from the data obtained, the average daily polyamine consumption of British adults was calculated to be in the range 350-500 pmol/person per d. The major sources of putrescine were fruit, cheese and non-green vegetables. All foods contributed similar amounts of spermidine to the diet, although levels were generally higher in green vegetables. Meat was the richest source of spermine. However, only a part of the polyamines supplied by the diet is available for use by the body. Based on experiments with rats it was established that polyamines were readily taken up from the gut lumen, probably by passive diffusion, and were partly metabolized during the process of absorption. More than 80% of the putrescine was converted to other polyamines and non-polyamine metabolites, mostly to amino acids. The enzyme responsible for controlling the bioavailability of putrescine was diamine oxidase (EC 1.4.3.6). For spermidine and spermine, however, about 7 W YO of the intragastrically intubated dose remained in the original form.Considering the limitations on bioavailability (metabolism and conversion), the amounts of polyamines supplied by the average daily diet in Britain should satisfy metabolic requirements.

The lectin, phytohaemagglutinin, present in beans survives passage through the gastrointestinal tract in a biologically and immunologically intact form. It is known that by binding to the brush border membranes of the small intestine phytohaemagglutinin induces its hyperplastic growth. However, its effect on the other parts of the gut are not known. This study considered the dose and time dependent changes in the gastrointestinal tract exposed to phytohaemagglutinin. Lectin binding was detected by polyclonal antibodies using PAP staining to the surface and the parietal cell region of the stomach, the brush border epithelium of the small intestine, and to the surface membrane of the caecum and colon. To characterise the metabolic changes in the gut organ weights, protein, RNA, DNA, and polyamine contents were measured. While phytohaemagglutinin induced a dose and time dependent growth of the small intestine by lengthening the tissue and thickening the gut wall by increasing the number of crypt cells, the lectin also changed the size and metabolism of the large intestine and pancreas, but this growth was by hypertrophy. Phytohaemagglutinin in the diet influences the size, metabolism, and function of the entire digestive tract. The lectin induced changes were fully or partially reversed within three days. (Gut 1995; 37: 353-360)

The reversible and dose-dependent hyperplastic growth of the small intestine and accelerated epithelial cell turnover caused by feeding rats with diets containing kidney bean lectin (PHA) increased the proportion of immature cells on the villi whose membrane and/or cytoplasm contained mainly simple, polymannosylated glycans. These new alpha-linked mannosyl terminals, particularly of the damaged epithelium, facilitated the preferential adherence of opportunistic Escherichia coli with mannose-sensitive Type 1 fimbriae, and other coliforms, to the glycocalyx. Accordingly, the growth of the gut was accompanied by a reversible and PHA dose-dependent overgrowth with E. coli. As expected from their common carbohydrate specificity, the inclusion in the diet of the mannose-specific agglutinin from snowdrop (Galanthus nivalis) bulbs (GNA) significantly reduced the extent of E. coli overgrowth, but abolished neither the growth nor the damage caused by PHA to the small intestine. Thus, GNA and perhaps other mannose-specific lectins, especially when used in a preventive mode, can be used to specifically block the proliferation of Type 1 E. coli in the small intestine.

No abstract

Polyamines are ubiquitous molecules that occur in every living cell. They fulfil an array of roles in cellular metabolism [ 1,2] and are involved in many steps of protein, RNA and DNA synthesis, and are therefore essential for growth and cell proliferation. However, the most important function of polyamines is as mediators of the action of hormones and growth factors.It was thought that polyamines were synthesised in situ in the cells when required. However, as more and more information becomes available, the importance of polyamines from extracellular sources, particularly the diet or bacteria resident in the gastrointestinal tract, is increasingly recognised [3-51. On this basis, three different sources of polyamines for growth have been identified: a. in situ biosynthesis; b. daily dietary intake and c. contribution by colonic bacteria.It is difficult to assess the relative importance of these sources, but it is possible from body composition and the polyamine synthesis capacity of the different organs of rats to calculate the order of magnitude of the likely contribution by the diet and bacteria.Rat stock diet was analysed for polyamine content.Depending on the batch, standard laboratory rat diet (Purina) contained about 220-240 nmoledg putrescine, 230-240 nmoles/g cadaverine, 540-570 nmoleslg spermidine and 100-130 nmoles/g spermine. Based on this data, a 100 g rat, fed ad libitum on stock diet, consumes about 17-18 g food daily, supplying approximately 4 pmoles putrescine, 4.1 pmoles cadaverine, 9.7 pmoles spermidine and 2 pmoles spermine. By giving 14C-polyamines to rats by intragastric intubation, we found that polyamines enter the systemic circulation, so food appears to constitute a natural source of polyamines. Although the catabolic enzymes diamine oxidase and polyamine oxidase might limit polyamine bioavailability, about 20-30% of putrescine and 70-80% of the dietary spermidine and spermine might be available for uptake per day [6].Different types of food, based on the 'normal' UK diet [7], were analysed by HPLC to determine their polyamine content. All contained polyamines and the 'normal' diet for an adult in the UK would provide about 220 pmoles putrescine, 100 pmoles spermidine and 70 pmoles spermine [6].However, it is not known how much of these dietary polyamines can be absorbed and made available for utilisation by either the rat or human body.Four enzymes are involved in polyamine biosynthesis: ornithine decarboxylase (ODC), adenosyl-L-methionine decarboxylase (SAM DC) and the spermidine and spermine synthases, with ODC and SAM DC considered to be the ratelimiting enzymes. Enzyme activity can increase dramatically in rapidly proliferating cells under a variety of conditions, generating high levels of polyamines [1,8]. Unfortunately, in the literature ODC and polyamine levels in rats are not always given in comparable forms. In the present work, mean protein values and organ weights were used to calculate the total concentrations so that the data in Table 1 are only estimates of what might ...