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Biomedical subjects

S Innami

Publications and source records attributed to S Innami.

At least 37 records · Page 2Linked to original sources
PubMed1990

Effect of polychlorinated biphenyls on tissue distribution and intestinal absorption of alpha-tocopherol in rats.

We conducted experiments to elucidate the mechanism by which alpha-tocopherol (alpha-toc) concentration in the liver remarkably increases in rats treated with polychlorinated biphenyls (PCB) when excess amounts of DL-alpha-tocopheryl-acetate (alpha-toc-ac) were given. First, diets containing 5 and 50 mg of alpha-toc-ac per 100 g were respectively added with 0.05% of PCB and given to rats for 10 days, and alpha-toc distributions in tissues were determined. Next, the disappearance of alpha-toc from a ligated intestine of vitamin E (E)-deficient rats was then studied. There were no significant differences between the control and the PCB groups in alpha-toc concentrations in the liver and other tissues except a few tissues when a lower level of alpha-toc-ac (5 mg) was given. Conversely, when a higher level of alpha-toc-ac (50 mg) was given, alpha-toc concentration in the liver of the PCB group significantly increased compared to that of the control group. This agrees with the result previously reported, showing a remarkable reproducibility. In addition, alpha-toc concentrations in tissues other than the liver were also significantly higher in the PCB group than in the control group. Transmigration of alpha-toc to the liver from other tissues was therefore excluded. The alpha-toc absorption test using the ligated intestine of E-deficient rats revealed that alpha-toc disappears from the intestine at a higher rate in the presence of PCB compared to the untreated control group. This may indicate that alpha-toc absorption by passive diffusion is accelerated in the coexistence of PCB.

Animals↗
PubMed1990

Influence of vitamin B2 deficiency on polychlorinated biphenyls-induced liver lipid peroxides formation in rats.

The present study is carried out to explore whether the liver microsomal drug-metabolizing enzymes induced by PCB are associated with the PCB-induced liver lipid peroxide formation in rats. For this purpose, variations of the drug-metabolizing enzyme activities mediated by vitamin B2 deficiency were utilized. The administration of PCB to rats induced the liver microsomal cytochrome P-450 and vitamin B2 deficiency promoted the induction. The cytochrome b5 was also induced by PCB but no further induction by vitamin B2 deficiency was observed. The flavoenzyme, NADPH-cytochrome c reductase, was induced by PCB when the vitamin B2-supplemented PCB diet was fed to rats, but the activity of the enzyme was decreased by vitamin B2 deficiency and PCB further decreased the activity. The liver lipid peroxide levels increased in PCB groups with and without vitamin B2 compared with each PCB-free group, but the lipid peroxide level in vitamin B2-deficient PCB group was significantly lower than in vitamin B2-supplemented PCB group. From these results, the PCB-induced liver lipid peroxide formation was not necessarily related to the variations of the liver microsomal drug-metabolizing enzymes.

Animals↗
PubMed1984

Differential effects of dietary eicosapentaenoic and docosahexaenoic fatty acids on lowering of triglyceride and cholesterol levels in the serum of rats on hypercholesterolemic diet.

This investigation was attempted in order to further clarify the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on lipid metabolism in rats. Ninety-three percent ethyleicosapentaenoate (EPAconc) and 91% ethyl-docosahexaenoate (DHAconc) were used and supplied at the 3% level to a hypercholesterolemic basal diet which contained 5% lard. Four experimental diets were prepared from (1) 5% olive oil, (2) 2% olive oil +3% ethyl-linoleate, (3) 2% olive oil +3% EPAconc, and (4) 2% olive oil +3% DHAconc plus hypercholesterolemic basal diet. Young male rats were fed on these diets for respective periods of 10 and 20 days. Concentrations of serum lipids in rats fed on the diets (2), (3) and (4) were compared to those of the control group (diet (1]. Serum total cholesterol level was significantly lower only in the animals fed on DHAconc, whereas serum triglyceride concentration was significantly lower only in the animals fed on EPAconc. Serum phospholipid level was significantly lowered both in the animals fed on either EPAconc or DHAconc. Serum lipid peroxide concentration was elevated in these two groups of animals, while serum alpha-tocopherol concentration was lower in both groups of animals fed on EPAconc and DHAconc, respectively, although these findings were less marked in the rats on the EPAconc diet. From these findings, it is postulated that EPA and DHA have different effects on lipid metabolism in rats with hypercholesterolemia experimentally induced.

Animals↗
PubMed1984

Effect of indigestible polysaccharides on pancreatic exocrine secretion and biliary output.

The present study was designed to determine the effect of purified viscous polysaccharides on pancreatic exocrine secretion and biliary output. Male Sprague-Dawley rats aged 5 weeks were fed either on the control diet which contained no fiber or on the experimental diets that contained 5% indigestible polysaccharides (agar, kappa-carrageenan, Na-alginate and konjac mannan). After pretreatment with each diet for 2 weeks, the diet was discontinued overnight, and the animals were then allowed to eat 4 g of the test diet in 1 h. Immediately after this, a polyethylene tube was placed in the common bile duct, under anesthesia. Combined, free drained pancreatic-bile juice was collected for the following 1 h. Long-term (2 weeks) administration of Na-alginate and konjac mannan gave rise to increases in the volume of secreted juice and in the output of total bile acids, amylase and protease, whereas that of agar and kappa-carrageenan had no affect. Since a single dose of Na-alginate and konjac mannan was ineffective as regards pancreatic-bile secretion, the elevated secretion observed over prolonged periods may result from processes of adaptation against highly viscous polysaccharides.

Alginates↗
PubMed1983

Dietary effect of omega-3 type polyunsaturated fatty acids on serum and liver lipid levels in rats.

The dietary effect of omega-3 type highly polyunsaturated fatty acid concentrate (PUFA mix) was investigated on cholesterol and triglyceride levels in the serum and liver, and high density lipoprotein cholesterol (HDL-cholesterol) levels in the serum. The PUFA mix prepared from squid liver oil contained about 75% of total omega-3 type fatty acids. In rats fed the normal diet to which 3% PUFA mix was added, the levels of triglyceride, total cholesterol and phospholipid in the serum markedly decreased as compared to rats fed a 3% methyl-oleate diet. However, lipid peroxide values in the liver and serum increased in rats fed PUFA mix-diets. In the hypercholesterolemic rats, a 5% PUFA mix-diet caused growth retardation and a corresponding reduction in food intake. Lipid peroxide in the liver and serum were more elevated in rats fed diets containing 1, 3 and 5% PUFA mix than in rats fed diets containing 5% oleate or 5% linoleate. In all the rats on PUFA mix-diets, there were depression of serum total cholesterol and elevation of serum HDL-cholesterol. The ratio of HDL-cholesterol to total cholesterol increased in proportion to the amounts of dietary PUFA mix. Total cholesterol level in the liver was depressed after PUFA mix feeding.

Animals↗
PubMed1983

Effect of the degradation of cytochrome P-450 heme by secobarbital on polychlorinated biphenyls (PCB)-induced hepatic vitamin A reduction and lipid peroxide formation in rats.

The present studies were conducted to characterize the relevance of a microsomal mixed function oxidase system to the polychlorinated biphenyls (PCB)-induced vitamin A reduction and endogenous lipid peroxide formation in the liver of rats. And also, this study dealt with an influence of scavengers on the hepatic lipid peroxide formation stimulated by PCB. Rats were given a 0.01% PCB diet supplemented with adequate nutrients, for 14 days. In an experiment, secobarbital was injected subcutaneously for the degradation of hepatic microsomal cytochrome P-450 heme. A marked liver enlargement and a significant increase of total liver lipid content were observed in the PCB group. The secobarbital enhanced the PCB-induced liver enlargement but no effect of secobarbital on the lipid content was recognized. PCB significantly induced hepatic microsomal cytochrome P-450, but not both cytochrome b5 and NADPH-cytochrome c reductase. The secobarbital suppressed the induction of cytochrome P-450 caused by PCB to approximately one-half. The hepatic vitamin A content significantly decreased on PCB administration and the secobarbital slightly enhanced the PCB-induced vitamin A reduction. However, the vitamin A content in the secobarbital-injected control group decreased to nearly the same levels as in the PCB groups. Therefore, it was presumed that the hepatic microsomal mixed function oxidase system, especially the cytochrome P-450, was possibly not directly involved in the PCB-induced hepatic vitamin A reduction or that a metabolic system related to mixed function oxidase system was involved in the reduction. On the other hand, the hepatic lipid peroxide content tended to increase on PCB administration though no significant difference was recognized. In contrast, the hepatic lipid peroxide content significantly increased in the secobarbital-injected PCB group as compared with the secobarbital-injected control group. However, there was no difference in the lipid peroxide contents between the control groups with and without the injection of secobarbital, and also between the PCB groups. The hepatic vitamin E contents lowered in the secobarbital-injected groups but no effect was observed on PCB administration. The glutathione peroxidase activity decreased significantly on PCB administration and the secobarbital further decreased the activity. Therefore, it was suggested that the significant increase and tendency of increase in hepatic lipid peroxide contents in the PCB groups with and without injection of secobarbital were ascribed to an insufficiency of lipid peroxide scavengers in the liver.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1976

Further studies on the reduction of vitamin A content in the livers of rats given polychlorinated biphenyls.

Further investigations on the reduction of vitamin A content in the liver of rats fed a 0.1% PCB diet were conducted. The first experiment, in which rats were fed a 0.1% PCB diet for 8 weeks and vitamin A in the liver was determined at 2-week intervals, suggested that a significant decrease of vitamin A in the liver might occur within 2 weeks of PCB ingestion. In the second experiment a significant reduction of vitamin A content per gram of liver, but not per whole liver, in rats fed a 0.1% PCB diet was observed on the 3rd day of PCB ingestion, and then on the 6th day the difference between the control group and the PCB-fed group became much more remarkable. But thereafter no further reduction was seen, indicating a lower limit of vitamin A concentration in the liver of rats fed PCB. It was found that retinol binding protein in the serum of rats fed the 0.1% PCB diet decreased to one-half that of the control group on the 10th day of PCB ingestion, suggesting also a marked reduction in serum vitamin A level. Another experiment revealed that a decrease in hepatic vitamin A occurred even at low PCB levels, but serum phospholipid did not respond at all to any PCB level examined until 7 days after PCB ingestion began. The mechanisms of sensitive response of vitamin A in the animals fed PCB are briefly discussed.

Animals↗