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Biomedical subjects

C Y Ho

Publications and source records attributed to C Y Ho.

69 records · Page 4Linked to original sources
PubMed1983

Homogenized bovine milk xanthine oxidase: a critique of the hypothesis relating to plasmalogen depletion and cardiovascular disease.

A hypothesis has repeatedly been promoted that xanthine oxidase from homogenized bovine milk is absorbed intact, damaging cardiovascular tissue by depleting plasmalogens and initiating atherosclerotic changes that culminate in heart disease. In the light of recent experimental evidence, the present paper examines the validity of this hypothesis and associated claims. The evidence leads to the conclusion that 1) absorption of dietary xanthine oxidase has not been demonstrated; 2) a relationship between intakes of homogenized milk and levels of serum xanthine oxidase activity have not been established; 3) a direct role for xanthine oxidase in plasmalogen depletion has not been established; 4) neither liposome formation during homogenization of milk nor absorption of intact liposomes from the gastrointestinal tract has been demonstrated; and 5) data are lacking to support the claim that large doses of folic acid inhibit xanthine oxidase in vivo and/or are therapeutic in heart disease. Experimental evidence has failed to substantiate, and in many cases has refuted, the xanthine oxidase/plasmalogen depletion hypothesis.

Animals↗
PubMed1980

Metabolism of orally and intravenously administered purines in rats.

One experiment was conducted in which radioactively labeled purine bases (adenine, guanine, hypoxanthine and xanthine) were individually given intravenously to young adult rats and the recovery of radioactivity in urine and gut, gut content and liver was measured at the end of the next 24 hours. The total recovery of radioactivity from orally and intravenously administered adenine was measured in experiment 2. A third experiment measured the recoveries of radioactivity from oral and intravenous adenine in a wider variety of tissues and organs than in experiment 1. The chemical identities of the urinary end products of the metabolism or orally and intravenously administered adenine were compared in a fourth experiment. When purines were given intravenously, significantly more of the administered radioactivity was recovered in urine from rats given guanine, hypoxanthine or xanthine compared with those given adenine. The greater recoveries of radioactivity in urine were associated with smaller recoveries in tissues. A larger proportion of intravenously compared to orally administered radioactivity from adenine was incorporated into all body tissues, and this was most pronounced in glandular and lymphoid tissues. The primary urinary end product of both orally and intravenously administered adenine was allantoin. The absorption of individual purines from isolated rat gut sacs was evaluated in a fifth experiment. A significant proportion of unaltered adenine crossed the mucosal to serosal barrier of intestinal sacs whereas unaltered guanine, hypoxanthine or xanthine did not cross into the serosal fluid. These results show that the intestinal metabolism of dietary adenine is uniquely different from that of guanine, hypoxanthine or xanthine.

Adenine↗
PubMed1979

Immunological similarities of mammalian xanthine oxidases.

The degree of relatedness among mammalian xanthine oxidases (XO) was determined by microcomplement fixation. Rabbit anti bovine milk XO serum was tested against xanthine oxidase (homologous protein) and against the heterologous proteins of bovine liver, monkey liver, rat liver, lactating cow serum, nonlactating cow serum, and steer serum. The indices of dissimilarity for the heterologous proteins were expressed as units of immunological distance and the percent sequence differences among these proteins inferred from the y = 5x relationship where y is immunological distance and x is percent sequence difference. Rat liver XO differed by approximately 27% in amino acid sequence from bovine milk XO. In order of increasing immunological distance from bovine milk XO, the sources of XO ranked as follows: lactating cow serum less than nonlactating cow serum less than steer serum = beef liver less than monkey liver less rat liver. The monkey ranked much closer than the rat in order of phylogenetic kinship to the cow. Starch gel electrophoresis of liver, milk, and serum showed that the milk and the serum contained only cationic forms of xanthine oxidase while all the liver samples tested contained cationic as well as anionic forms of the enzyme. The electrophoretic mobility properties of xanthine oxidase confirmed the polymorphic nature of the enzyme as revealed by the immunological data.

Animals↗
PubMed1977

Bovine milk xanthine oxidase, blood lipids and coronary plaques in rabbits.

The effects of prolonged intravenous administration of bovine milk xanthine oxidase (EC 1.2.3.2.) on blood lipids and arterial integrity were measured to determine if the administration of this enzyme produces metabolic changes conducive to plaque formation. New Zealand White rabbits were injected intravenously with bovine milk xanthine oxidase at 4-day intervals during a 13-week test period. At the end of the test period, the rabbits were killed and blood, heart, aorta, liver, and kidneys were collected and evaluated. Rabbits injected with phosphate buffer or acid-denatured xanthine oxidase for the same length of time served as negative controls. Additional rabbits fed a diet containing 3% added cholesterol for the same time period served as positive controls. The administration of xanthine oxidase in large amounts over a prolonged period did not alter serum cholesterol or triglyceride levels and did not reduce plasmalogen levels in the aorta or heart. Xanthine oxidase administration did not induce arterial plaque formation. Cholesterol feeding over the same time period increased serum cholesterol levels, reduced liver xanthine oxidase activity levels and resulted in a marked development of arterial plaques. Althouth xanthine oxidase activity was found in liver from all rabbits, enzyme activity was not detectable in aorta, heart or kidneys from any rabbit. Free or complexed bovine milk xanthine oxidase could not be demonstrated in heart, aorta, liver or kidneys from any of the rabbits with immunodiffusion or with immunofluorescent techniques. The study showed that when large intravenous doses of bovine milk xanthine oxidase were given to rabbits, the enzyme was not deposited in heart, aorta, liver or kidneys. The study also showed that large intravenous doses of xanthine oxidase over prolonged periods did not deplete arterial or coronary tissue plasmalogens, and did not induce arterial plaque formation.

Animals↗
PubMed1976

Penguin evolution: protein comparisons demonstrate phylogenetic relationship to flying aquatic birds.

Quantitative immunological comparisons of three avian proteins, transferrin, ovalbumin, and penalbumin, indicate that penguins are phylogenetically most closely related to loons, albatrosses, herons, and grebes. These data support the theory that the ancestors of penguins were flying oceanic birds and that flightlessness in penguins has evolved independently from flightlessness in ratites.

Amino Acid Sequence↗
PubMed1976

Digestion and absorption of bovine milk xanthine oxidase and its role as an aldehyde oxidase.

The effects of acidic and intestinal proteolytic environments on bovine milk xanthine oxidase (XO) activity were determined in order to evaluate the extent to which this enzyme was absorbed in biologically active form. The inhibition of XO by folic acid and the relative affinities of XO for the oxidation of palmitaldehyde, stearaldehyde, and xanthine were compared. The effects of acid and gastric juice on XO activity were measured by incubating purified enzyme, and non-purified enzyme (milk), in buffers ranging in pH from 2 to 9. Fresh gastric juice was also incubated with milk. Increasing amounts of the enzyme were inactivated as the pH of the incubation mixture was reduced below pH 6.5. Below pH 3.5, the enzyme was completely inactivated. Gastric juice, pH juice incubated with milk. Milk XO activity was reduced 36% when mild was incubated with an equal volume of gastric juice. Homogenized milk had 59% less XO activity compared with raw molk. Fresh raw milk XO, homogenized milk XO, and purified XO were equally susceptible to inactivation by acid or gastric juice. After incubation of milk with gastric juice, or gastric juice followed by pancreatin, XO activity was associated with a macromolecule of 300,000 daltons molecular weight and subunits containg activity were not found. It was estimated that 0.00008% of the XO in the intestine was absorbed. Both folic acid and allopurinol inhibited XO activity in vitro. Allopurinol was 3.5 times more potent an inhibitor than folic acid. A large excess of dietary folic acid did not reduce rat liver or intestinal XO activity in vivo. XO had a much greater affinity for xanthine than for palmitaldehyde or stearaldehyde substrates. It was estimated that of 100 mg of XO in fresh raw milk, 41 mg remained after homogenization, 27 mg entered the intestine and only 20 ng were absorbed as intact enzyme.

Absorption↗
PubMedDate not supplied

Opposing effects of sodium salicylate and haematopoietic cytokines IL-3, IL-5 and GM-CSF on mitogen-activated protein kinases and apoptosis of EoL-1 cells.

Haematopoietic cytokines such as IL-3, IL-5 and GM-CSF not only activate eosinophils but also prolong their life span by inhibiting their apoptotic cell death. We have studied the effects of IL-3, IL-5 and GM-CSF on apoptosis and mitogen-activated protein kinases (MAPKs) in a human eosinophilic leukaemic cell line (EoL-1). Results demonstrated that all three cytokines could trigger the receptor-mediated activation of extracellular signal-regulated kinase (ERK) within one hour but not p38 MAPK activity in EoL-1 cells. In contrast, sodium salicylate (NaSal), a nonsteroidal anti-inflammatory drug (NSAID), could activate p38 MAPK but not ERK within one hour. Both cytokines and specific p38 MAPK inhibitor SB 203580 could partly block the NaSal-induced apoptosis in EoL-1 cells. A specific MAPK/ERK kinase (MEK) inhibitor, PD 098059, could induce apoptosis and eliminate the protective effect of IL-3, IL-5 and GM-CSF against NaSal-induced apoptosis in EoL-1 cells. Taken together, cytokines IL-3, IL-5 and GM-CSF could prolong EoL-1 cells survival through the transient activation of ERK. On the other hand, activation of p38 MAPK in EoL-1 cells by NaSal could lead to apoptosis. Activation of p38 MAPK and the resulting induction of apoptosis in EoL-1 cells may be important to explain the anti-inflammatory action of NSAID in allergic inflammation.

Animals↗