Short-chain fatty acids (SCFAs), namely butyrate, acetate and propionate, originate from the bacterial fermentation of dietary fibers and are the predominant anions present in the large bowel. Our study was carried out to investigate the effects of SCFAs on growth of the human adenocarcinoma cell line, HT29. The results show that, under our culture conditions, both propionate and butyrate inhibit growth of HT29 cells, whereas acetate has no significant effect. The antiproliferative effect of propionate or butyrate is associated with an inhibition of FCS-induced activation of ornithine decarboxylase (ODC), a key enzyme of polyamine metabolism. Inhibition of growth induced by either propionate or butyrate is not reversed by the addition of putrescine, which reveals that these SCFAs are not acting solely on the ODC/polyamine system. Our data show that propionate and butyrate, unlike acetate, induce an increase in alkaline phosphatase activity, which reflects a more differentiated phenotype than that of untreated control cells. Taken together, our results suggest that propionate, like butyrate, may play an important role in the physiology of the colon and could partially account for the protective effect of dietary fibers with respect to colon carcinogenesis.

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For determination of (chiefly) glycogen content, tissue homogenates in citrate buffer are mixed with exo-1,4-α-glucosidase (EC 3.2.1.3). Liberated glucose is estimated with a Beckman Glucose Analyzer. This method was checked with commercial glycogen (from oysters) and with fish (carp) tissues. Comparative measurements were made with the classic Good-Kramer-Somogyi method [J. Biol. Chem. 100, 485 (1933)]. The described method, suitable for small samples of tissue, such as those obtained by biopsy, seems to be simple and accurate, but gives values 5 to 10% higher than those given by the classic KOH-ethanol method.

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Cellular mechanisms underlying the expression of stress proteins (HSP) were studied in the human cell-line A549 submitted to a pollutant, cadmium, in the presence of several agents which modulate the glutathione level and, supposedly, the effects of this metal in the cell. It was observed that HSP 90, HSP 72 and HSP 27 are significantly over-expressed after exposure to cadmium chloride for 24 h. Low cadmium concentrations (i.e. from 1 to 10 microM) also triggered a slight accumulation of glutathione, whereas this compound was depleted after exposure to higher cadmium concentrations (25-100 microM). When 50 microM diethyl-maleate, which traps glutathione, was added together with cadmium, the over-expression of HSP 72 and HSP 90 was much stronger. Treatment of cells with 20 or 40 mM N-acetyl-L-cysteine, which traps free radicals, was found to increase by 30% the glutathione level and to suppress the HSP over-expression. From our results, it is suggested that HSP induction by cadmium in A549 cells is due, at least in part, to the oxidative stress consisting in formation of reactive oxygen species and inhibition of peroxides detoxification. Due to this oxidative status within the cell, more proteins would be damaged inducing the HSP over-expression.