Previously we have observed increased specific activities of several lysosomal hydrolases in scorbutic guinea pigs and thus the specificity of this effect was examined in guinea pigs marginally deficient in ascorbic acid (AA). Guinea pigs were fed an AA-deficient diet for 2 weeks to deplete body AA pools and then fed a stock diet containing 0.5 mg AA/g diet or the deficient diet plus oral administration of 10 mg AA/day, 1 mg AA/100 g body weight or 0.5 mg AA/100 g body weight each day. Animal were periodically killed during the 12-week experiment and lysosomes isolated from individual livers and analyzed. Serum and brain AA declined when AA was withheld, returned to normal when the stock diet or 10 mg AA were fed but remained at low levels on administation of 1.0 mg or 0.5 mg AA/100 g body weight. Brain norepinephrine followed a similar pattern to brain AA and was opposite to the pattern observed for dopamine. In guinea pigs receiving 1 mg AA/100 g body weight, amine concentrations slowly returned to normal after 8 weeks. Serum hexosaminidase and lysosomal cathepsins A and B were unchanged during the experiment, whereas lysosomal hexosaminidase and acid phosphatase were significantly higher when the experiment was terminated.
The effects of L-ascorbic acid deficiency on guinea pig hepatic and brain lysosomal hydrolases were examined. In general, hepatic beta-N-acetylhexosaminidase, beta-D-glucoronidase, alpha-D-galactosidase, alpha-D-mannosidase, and acid phosphatase were elevated in scorbutic animals. This appears to be independent of the starved state. Brain beta-D-glucoronidase and acid phosphatase followed a similar pattern to that observed with the liver enzymes, but brain beta-N-acetylhexosaminidase was not affected by L-ascorbic acid decreased the activity of hepatic beta-N-acetylhexosaminiadase was unaffected by dietary treatments although the activity of beta-N-acetylhexosaminidase A tended to increase in the scorbutic animals. Subcellular fractions were obtained from the three groups of animals and the recoveries of protein, beta-N-acetylhexosaminidase, and glucose-6-phosphatase estimated.
Groups of 20 female Sprague-Dawley rats were given a single oral 5 mg dose of 7,12-dimethylbenz(a)anthracene at 50 days of age, and one week later were transferred from a Purina Chow diet to purified diets containing 68% by weight of sugar (dextrose or sucrose) or starch (wheat, rice or potato starch) and 5% by weight of fat. Sucrose and wheat starch were also fed at a level of 49% in a diet containing 20% fat. Rats fed the sugar diets developed significantly more mammary tumors than those fed the starch diets, at both low and high levels of dietary fat. These results are consistent with epidemiological data showing that age-adjusted breast cancer mortality in humans is positively correlated with sugar intake and negatively correlated with intake of complex carbohydrates.
Rat alveolar macrophages separated into four isopycnic fractions on Percoll gradients were functionally heterogeneous in bacterial phagocytosis, intracellular killing, superoxide anion release, and lysosomal enzyme activity but not in hydrogen peroxide release. With increasing alveolar macrophage density, phagocytosis, intracellular killing, superoxide anion release, and lysozyme activity increase, and acid hydrolase activity decreases.
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