Beneficial effects of judo training on bone mineral density of high-school boys in Korea.

Bone mineralization is strongly stimulated by weight-bearing exercise during growth and development. Judo, an Olympic combat sport, is a well-known form of strenuous and weight-bearing physical activity. Therefore, the primary goal of this study was to determine the effects of Judo practice on the bone health of male high school students in Korea. The secondary goal of this study was to measure and compare the bone mineral density (BMD) of the hands of Judo players and sedentary control subjects. Thirty Judo players (JDP) and 30 sedentary high school boys (CON) voluntarily participated in the present study, and all of the sedentary control subjects were individually matched to the Judo players by body weight. BMD was determined by using dual-energy X-ray absorptiometry (Hologic, Bedford, MA, USA). The lumbar spine, femur and forearm BMD in the JDP group were significantly greater by 22.7%, 24.5%, and 18.3%, respectively, than those in the CON group. In addition, a significant difference in the CON group was observed between the dominant hand (DH) radius (0.710 ± 0.074 g/cm(2)) and the non-dominant hand (NDH) radius (0.683 ± 0.072 g/cm(2)), but this was not observed in the JDP group (DH = 0.819 ± 0.055 g/cm(2); NDH = 810 ± 0.066 g/cm(2)) (P < 0.05). Therefore, the results of this study suggest that Judo practice during the growth period significantly improves bone health in high school male students. In addition, it seems that Judo practice could eliminate the effect of increased BMD in the dominant hand.

Feeding of a low-zinc diet lowers the tissue concentrations of alpha-tocopherol in adult rats.

Previous work has shown that a low dietary intake of zinc for a short duration significantly lowers the lymphatic absorption of alpha-tocopherol (alphaTP) in adult male rats. The present study investigated whether the nutritional status of zinc is critical in maintaining the tissue levels of the vitamin. One group of rats was fed an AIN-93G diet containing 3 mg zinc/kg (low zinc, LZ) and the other was fed the same diet but containing 30 mg zinc/kg (adequate zinc, AZ). Food intakes between groups were matched by feeding two meals per day. At 6 wk, the body weights (356+/-8 g) of LZ rats reached 98% those (362+/-10 g) of AZ rats. Feeding of the LZ diet for 6 wk significantly lowered the concentrations of both alphaTP and zinc in the liver, kidney, heart, testis, and brain. No consistent relationships between alphaTP and zinc concentrations were observed in other tissues such as spleen, lung, gastrocnemius muscle, and retroperitoneal fat tissues. The concentrations of alphaTP in the liver, testis, brain, spleen, heart, and kidney were significantly correlated with the tissue concentrations of zinc. The LZ diet slightly but significantly increased the total lipid contents (mg/g) of liver, kidney, heart, and spleen. However, the tissue levels of phospholipid (micromol/100 mg lipid) in the heart, lung, testis, and spleen were decreased significantly in LZ rats. These findings indicate that low zinc intake results in a pronounced decrease in the animal's alphaTP status under the conditions of matched food intakes, body weights, and feeding patterns. The lower tissue levels of alphaTP may explain in part the compromised antioxidant defense system and increased susceptibility to oxidative damage observed in zinc deficiency.

Egg phosphatidylcholine decreases the lymphatic absorption of cholesterol in rats.

This study was conducted to determine the effects of phosphatidylcholine (PC) from different sources on intestinal absorption of cholesterol. Male Sprague-Dawley rats were fed an AIN-93G diet containing soybean oil for 4 wk. Each rat with lymph cannula was infused via a duodenal catheter at 3.0 mL/h for 8 h with a lipid emulsion [in micromol: 451.8 triolein, 27.8 kBq 14C-cholesterol (CH), 20.7 CH, 3.6 alpha-tocopherol, and 100 PC in 24 mL PBS, pH 6.6]. The PC in the lipid emulsion was egg PC (EPC), hydrogenated egg PC (HPC), or soy PC (SPC). The EPC in the lipid emulsion markedly lowered the lymphatic absorption of 14C-CH (24.7 +/- 2.5% dose) compared with SPC (34.9 +/- 1.2%) and a lipid emulsion containing no PC (NPC) (30.8 +/- 2.0%). The HPC further lowered the absorption of 14C-CH to 21.1 +/- 1.4% dose. The outputs of phospholipid were unaffected by the source of PC infused (EPC, 32.2 +/- 1.7; HPC, 31.8 +/- 1.6; and SPC, 32.9 +/- 1.8 micromol/8 h). Compared with NPC (595.0 +/- 59.5 micromol), the total output of fatty acids over 8 h was increased significantly by SPC (685.4 +/- 55.8 micromol), but decreased by HPC (467.7 +/- 28.4 micromol). The total lymphatic output of oleic acid (18:1), the major fatty acid infused in the form of triolein, did not differ among the NPC (448.0 +/- 58.2 micromol/8 h), SPC (457.9 +/- 52.3 micromol/8 h) and EPC (412.9 +/- 20.8 micromol/8 h) groups, but was significantly lower in the HPC group (262.0 +/- 24.1 micromol/8 h). The findings provide the first evidence that EPC markedly lowers the lymphatic absorption of cholesterol under in vivo conditions. The inhibitory effect of EPC appears to be due to the higher degree of saturation of its acyl groups relative to SPC, suggesting that the intestinal absorption of egg cholesterol may be reduced by the presence of PC in egg yolk.

Enteral infusion of phosphatidylcholine increases the lymphatic absorption of fat, but lowers alpha-tocopherol absorption in rats fed a low zinc diet*

Our previous study has shown that the lymphatic absorption of both fat and alpha-tocopherol (alphaTP) is lowered markedly in rats fed a low zinc diet, with a parallel decrease in lymphatic phospholipid (PL) output. This study was conducted to determine if enteral infusion of phosphatidylcholine (PC) could restore lymphatic absorption of fat and alphaTP in zinc-deficient rats. One group of rats was fed an AIN-93G diet containing 3 mg Zn/kg (low zinc; LZ) and the other was fed the same diet but containing 30 mg Zn/kg (adequate zinc; AZ). Rats were trained to consume two meals daily of equal amounts of food. At 6 wk, each rat with lymph fistula was infused at 3 mL/h with a lipid emulsion containing 3.6 &mgr;mol alphaTP and 565 &mgr;mol [carboxyl-14C]-triolein (14C-OA), with or without 40 &mgr;mol 1,2-dilinoleoyl-PC in 24 mL PBS at pH 6.4. The lymphatic absorptions of fat and alphaTP were determined by measuring 14C-radioactivity and alphaTP appearing in the mesenteric lymph collected hourly for 8 h. When the emulsion devoid of PC was infused, the absorptions of both 14C-OA (41 +/- 4% dose) and alphaTP (431 +/- 55 nmol) in LZ rats were significantly lower than in AZ rats (48 +/- 2% 14C-OA dose and 581 +/- 70 nmol alphaTP). When the emulsion containing PC was infused, the absorption of 14C-OA was restored rapidly to normal in LZ rats, along with a parallel increase in lymphatic PL output. However, PC infusion further lowered the absorption of alphaTP to 311 +/- 20 nmol/8 h in LZ rats and also lowered the absorption of alphaTP in AZ rats (347 +/- 48 nmol/8 h). The results demonstrate that low zinc intake results in impaired intestinal absorption of both alphaTP and fat. The findings also indicate that PC significantly improves the intestinal absorption of fat, but inhibits alphaTP absorption, suggesting that PC affects the intestinal absorption of alphaTP and fat via distinctly different mechanisms.

Intraduodenal infusion of lysophosphatidylcholine restores the intestinal absorption of vitamins A and E in rats fed a low-zinc diet.

Our previous work has shown that the lymphatic absorptions of lipids and lipid-soluble vitamins, retinol and alpha-tocopherol (alphaTP), are lowered markedly in rats fed a low-zinc (LZ) diet in parallel with lower lymphatic phospholipid outputs. Phosphatidylcholine (PC), when infused enterally, restored the absorptions of fat and retinol, but further lowered the absorption of alphaTP in rats fed the LZ diet. This study was conducted to determine whether a luminal infusion of lysophosphatidylcholine, a product of PC hydrolysis by pancreatic phospholipase A2 (PLA2), would simultaneously restore the absorptions of retinol and alphaTP in LZ rats. Rats were trained to consume two meals per day and were divided into two groups. One group was fed an AIN-93G diet containing a LZ (3.0 mg Zn/kg), and the other was fed the same diet, but containing adequate zinc (AZ; 30.0 mg Zn/kg) for 6 weeks. Rats with lymph cannula were infused at 3.0 ml/hr for 8 hr with a lipid emulsion containing retinol, alphaTP, and 14C-labeled triolein (14C-oleic acid) with or without 1-oleoyl-2-hydroxy phosphatidylcholine (lysoPC) in 24 ml of PBS (pH 6.5). When the lipid emulsion without lysoPC was infused, the absorptions of retinol and alphaTP were significantly lower in LZ rats (retinol, 13.2+/-1.5 nmol; alphaTP, 430.6+/-66.8 nmol) than in AZ rats (retinol, 18.2+/-1.0 nmol; alphaTP, 543.8+/-58.9 nmol). The lower absorptions of the vitamins in LZ rats occurred in parallel with a significant decrease in 14C-oleic acid absorption. When the emulsion containing lysoPC was infused, however, absorptions of the vitamins (retinol, 18.4+/-3.0 nmol; alphaTP, 777.2+/-92.1 nmol) in LZ rats were restored completely to the control levels (retinol, 20.4+/-2.8 nmol; alphaTP, 756.3+/-136.1 nmol). The results suggest that the luminal hydrolysis of PC to lysoPC by PLA2 may be impaired in LZ rats, resulting in impaired absorption of fat and the fat-soluble vitamins.

Phosphatidylcholine inhibits and lysophosphatidylcholine enhances the lymphatic absorption of alpha-tocopherol in adult rats.

This study was conducted to compare the effects of enterally infused phosphatidylcholine (PC) and lysophosphatidylcholine (lysoPC) on the lymphatic absorption of alpha-tocopherol (alphaTP) in male rats. In expt. 1, bile-diverted rats with mesenteric lymph cannulas were infused at 3.0 mL/h for 8 h with a lipid emulsion containing 5.0 micromol alphaTP, 565 micromol 14C-triolein (14C-OA) and 396 micromol Na+-taurocholate with 80 micromol 1,2-dipalmitoyl PC (DPPC) or 1,2-dilinoleoyl PC (DLPC) or without PC (NoPC) in 24 mL phosphate-buffered saline (pH 6.6). In expt. 2, the effects of 1,2-dioleoyl PC (DOPC) and 1-oleoyl-2-hydroxy-PC (lysoPC) on alphaTP and 14C-cholesterol absorption were compared in rats with lymph cannulas. When DPPC or DLPC was infused, the lymphatic absorption of alphaTP was lowered drastically. The cumulative absorptions of alphaTP in rats infused with DPPC and DLPC were 45 and 52%, respectively, of the control values (NoPC). No significant difference was noted between the PC groups. In contrast, the absorption of 14C-OA was increased by 42 to 43% in rats infused with DPPC or DLPC compared with that in NoPC rats. Phospholipid outputs also were significantly higher in DPPC (34.0 +/- 5.5 micromol /8 h) and DLPC (32.4 +/- 2.4 micromol /8 h) rats than in NoPC rats (21.2 +/- 4.2 micromol /8 h). When lysoPC was infused, the absorptions of alphaTP and 14C-cholesterol were increased markedly compared with those for DOPC, with no significant difference in PL output between groups infused with DOPC and lysoPC. These observations provide clear evidence that PC present in a lipid emulsion inhibits alphaTP absorption, whereas it enhances the absorption of fat. The data also demonstrate that lysoPC simultaneously increases the absorption of alphaTP and cholesterol. The findings indicate that luminal PC inhibits the absorption of alphaTP and that hydrolysis of PC is critical to improving the intestinal absorption of the vitamin.

Augmented death in immunostimulated astrocytes deprived of glucose: inhibition by an iron porphyrin FeTMPyP.

The present study shows that under glucose-deprived conditions immunostimulated astrocytes rapidly undergo death due to their increased susceptibility to endogenously produced peroxynitrite. Fe(III)tetrakis(N-methyl-4'-pyridyl)porphyrin (FeTMPyP), but not the structurally related compounds ZnTMPyP and H(2)TMPyP, prevented the death in glucose-deprived immunostimulated astrocytes. Consistently, FeTMPyP, not ZnTMPyP and H(2)TMPyP, completely blocked the elevation of nitrotyrosine immunoreactivity (a marker of peroxynitrite) and the depolarization of the mitochondrial transmembrane potential in glucose-deprived immunostimulated astrocytes. The present data suggest that peroxynitrite may be associated with glial cell death during metabolic deterioration in the cerebral ischemic penumbra.

Estradiol replacement in ovariectomized rats increases the hepatic concentration and biliary secretion of alpha-tocopherol and polyunsaturated fatty acids.

Previously, we showed that estradiol replacement in ovariectomized rats produced prominent increases in serum and liver alpha-tocopherol (alphaTP). The present study was conducted to examine whether the estrogen-induced increase in the liver concentrations of alphaTP affects its biliary secretion and the fatty acid compositions of hepatic and biliary lipids. Ten ovariectomized rats were assigned to two groups: five rats were implanted subcutaneously with time-release estradiol pellets (OXE; 25 microg/day/rat) and five with placebo (OXP). Twice daily rats were pair-fed a modified AIN-93G diet containing soybean oil. At 5 weeks, bile was collected via a bile cannula hourly for 8 hours during duodenal infusion of a lipid emulsion (565 micromol triolein and 396 micromol Na-taurocholate/24 mL phosphate buffered saline, pH 6.45) at 3.0 mL/hr. During the 8-hour period, no difference was noted in the hourly rate of bile flow (0.95 mL/hr in OXE rats vs. 0.99 mL/hr in OXP rats). The biliary output of alphaTP for 8 hours was higher in OXE rats (51.6 +/- 3.6 nmol) than OXP rats (31.7 +/- 2.9 nmol). Likewise, the liver concentration of alphaTP was higher in OXE rats (81.9 +/- 3.5 nmol/g liver) than in OXP rats (53.3 +/- 7.4 nmol/g liver). The biliary secretion of phospholipids (PL) for 8 hours was significantly (P < 0.05) higher in OXE rats (55.1 +/- 4.9 micromol) than in OXP rats (42.3 +/- 4.7 micromol). Among the PL fatty acids, the outputs of 20:4 and 22:6n-3 were increased most markedly by estradiol replacement. The total outputs of 22:6n-3 for 8 hours in OXE and OXP rats were 2.95 +/- 0.20 micromol and 1.37 +/- 0.23 micromol, respectively. In the liver, the concentrations of PL 22:5n-3 and 22:6n-3 were elevated significantly in OXE rats. The present results suggest that estradiol may protect hepatic PL and membranes against oxidative damage by improving the liver status of alphaTP.

Marginal zinc deficiency lowers the lymphatic absorption of alpha-tocopherol in rats.

The present study was conducted to investigate whether the intestinal absorption of vitamin E is influenced by marginal zinc deficiency. Rats trained to meal feed were divided into two groups and fed a diet containing 3 mg Zn/kg [a low zinc (LZ group)] or pair-fed (PF controls a zinc-adequate diet (30 mg Zn/kg). At 5 wk, the body weight (352 +/- 5 g, mean +/- SD) of LZ rats was 98.5% of that of PF rats (357 +/- 8 g). Rats with lymph cannula were infused at 3 mL/h via a duodenal catheter with a lipid emulsion consisting of 568 micromol triolein, 3.56 micromol alpha-tocopherol (alphaTP) and 396 micromol Na+-taurocholate in 24 mL of phosphate-buffered saline (pH 6.4). Lymph was collected hourly for 8 h. The amounts of alphaTP absorbed into the lymph were determined by high-performance liquid chromatography (HPLC). The hourly rate of alphaTP absorption was significantly lower in LZ than in PF rats. A marked difference (P < 0.05) was clearly evident even at 1 h (1.8 +/- 1.2 nmol/h in LZ vs. 8.5 +/- 3.0 nmol/h in PF). The peak rate of absorption was significantly lower in LZ rats (67.1 +/- 16.7 nmol/h at 5 h) than in PF rats (95.9 +/- 7.7 nmol/h at 4 h). The total amounts of alphaTP absorbed in 8 h in LZ and PF rats were 391.1 +/- 54.4 nmol (11.0 +/- 1.5% dose) and 613.9 +/- 105.8 nmol (17.2 +/- 3.0% dose), respectively. The lymphatic absorption of alphaTP was correlated with the amounts of PL (r = 0.77, P < 0.05) released into the mesenteric lymph. The hourly outputs of phospholipid and oleic acid also were significantly lower in LZ rats than in PF rats up to 4 h (P < 0.05). The cumulative lymphatic outputs of phospholipid (PL) were 20.1 +/- 3.7 micromol/8 h in LZ and 27.0 +/- 3.9 micromol/8 h in PF rats (P < 0.05). These results show that the intestinal absorption of vitamin E is affected by the zinc status of rats. This observation along with our earlier finding of a lower intestinal absorption of retinol suggests that zinc nutriture has a profound effect on the intestinal absorption and body status of lipid soluble vitamins.