Differential effects of milk proteins, BSA and soy protein on 4NQO- or MNNG-induced SCEs in V79 cells.

The possible antimutagenic effects of five different proteins against the mutagen 4-nitroquinoline 1-oxide (4NQO) were assessed in a mammalian cell system, using the sister chromatid exchange (SCE) test in Chinese hamster cells (V79). For this purpose the proteins casein, bovine serum albumin (BSA), soy protein, total whey protein and beta-lactoglobulin were studied, as well as pepsin-hydrolysed casein. In addition, the effect of casein on 1-methyl-1-nitroso-3-nitroguanidine (MNNG) was studied. The proteins were tested at a concentration of 1.15% (w/v). Casein was studied over a concentration range of 0 to 1.15% (w/v). A non-toxic concentration was used for the mutagens. Casein hydrolysis by pepsin took place in vitro, simulating human stomach conditions, which resulted in 84% non-casein-N and 16% remaining casein-N. Casein significantly inhibited SCE induction by 4NQO (inhibition 78%, at 1.15% casein, P < 0.05) and by MNNG (83%, at 1.15% casein, P < 0.01). BSA also significantly inhibited 4NQO-induced SCEs (94%, at 1.15% BSA; P < 0.01). However, soy protein, the whey protein fraction of milk and beta-lactoglobulin showed no inhibitory effects. Pepsin-hydrolysed casein inhibited SCE induction by 4NQO and MNNG to a similar extent as non-hydrolysed casein. It is concluded that casein, its pepsin hydrolysis products and BSA may protect mammalian cells against certain genotoxic compounds, whereas other milk proteins, such as whey protein, beta-lactoglobulin and soy protein, do not have this protective action. Although the mechanism of antimutagenicity is unknown, it seems plausible that the protein acts as a blocking agent by chemical or physical interaction with the mutagens. The accessibility of protein molecules and the presence of nucleophilic binding sites may be decisive factors in determining antimutagenic properties of proteins.

Effect of lipids and aldehydes on gap-junctional intercellular communication between human smooth muscle cells.

Inhibition of intercellular communication is an important feature in the tumour promotion phase of a multistage carcinogenesis model. In atherosclerosis inhibition of cell-cell communication by atherogenic compounds, e.g., low density lipoproteins (LDL), also seems to be important. For testing atherogenic compounds we used an atherosclerosis relevant cell type, namely human smooth muscle cells. In order to investigate which part of the LDL particle would be involved in inhibition of metabolic co-operation between human smooth muscle cells in culture we tested several fatty acids and their breakdown products, namely aldehydes. Unsaturated C-18 fatty acids markedly influenced gap-junctional intercellular communication (GJIC), whereas saturated (C18:0, C16:0) and unsaturated fatty acids with > 20 carbon atoms did not inhibit GJIC. In the case of oleic and elaidic acid, orientation seemed important; however, after exposure to palmitoleic and palmitelaidic acid no differences were found. The most potent inhibitor of GJIC was linoleic acid, which inhibited GJIC by 75%. No correlation was found between degrees of unsaturation and ability to inhibit GJIC. Of the tested aldehydes, hexanal, propanal, butanal and 4-hydroxynonenal did significantly inhibit GJIC, while pentanal had no effect. Since modification of LDL was shown to be important in order for LDL to inhibit GJIC, these results show that fatty acids and their oxidative breakdown products may be of importance for the inhibition of GJIC by LDL.

Twenty-four-hour energy expenditure and substrate utilization in body builders.

Twenty-four--hour energy expenditure (EE) was measured by indirect calorimetry in 10 body builders and 10 lean control subjects of the same sex with similar age, height, and percent body fat. The study was performed to elucidate possible effects of strength training on energy metabolism and substrate utilization. Twenty-four--hour EE was higher in the body builders than in control subjects but was similar when adjusted for differences in fat-free mass. A higher 24-h nonprotein respiratory quotient (RQ) was found in the body builders. Because both groups were in energy balance, the higher RQ in the body builders can be attributed to a different habitual diet or may be explained by physiological differences.