Methods of Extracting Vitamin A from Liver

Hinds, F. C.; Peter, A. P.; Richards, G. E.

doi:10.2527/jas1968.2761678x

Cited by 12 publications

(5 citation statements)

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“…Bile was collected under pentobarbital anesthesia by inserting a plastic tube (PE 20, Intramedic; Clay Adams, Parsippany, N.J.) into the bile duct (11) and was stored at Ϫ20ЊC until analyzed. Liver biopsy specimens were frozen at Ϫ20ЊC for analysis of the retinol levels as previously described (9,19). Spleens were obtained aseptically, and mononuclear cell suspensions were prepared.…”

Section: Methodsmentioning

confidence: 99%

Vitamin A deficiency predisposes to Staphylococcus aureus infection

et al. 1996

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We have investigated the consequences of vitamin A deficiency in a rat model of T-cell-dependent and superantigen-mediated Staphylococcus aureus arthritis. After intravenous inoculation of enterotoxin A-producing staphylococci, the vitamin A-deficient rats showed a decreased weight gain compared with the paired fed controls despite equal food consumption. The control rats developed arthritis in the first few days after bacterial inoculation, with a peak frequency at day 5, and then gradually recovered; however, the frequency of arthritis in the deficient rats increased continuously during the experimental period. The prevalence of arthritis 18 days after bacterial inoculation was 86% among the vitamin A-deficient rats and 44% among the control rats. During this period, 3 of 10 deficient rats and 1 of 10 control rats died. Further in vitro analysis revealed that T-cell responses to S. aureus were significantly higher in the vitamin A-deficient rats than in the control animals. In contrast, B-cell reactivity, measured as immunoglobulin levels, autoantibody levels, and specific antibacterial antibody levels in serum, did not differ between the groups. Interestingly, the innate host defense mechanisms against S. aureus were also profoundly affected by vitamin A deficiency. Thus, despite a larger number of circulating phagocytic cells in the vitamin A-deficient group, the capacity to phagocytize and exert intracellular killing of S. aureus was significantly decreased in comparison with the control rats. Furthermore, serum from the vitamin A-deficient rats inoculated with Staphylococcus aureus displayed decreased complement lysis activity. Our results suggest that the increased susceptibility to S. aureus infection observed in the vitamin A-deficient rats is due to a concerted action of antigen-specific T-cell hyperactivity, impaired function of the phagocytes, and decreased complement activity.

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Section: Methodsmentioning

confidence: 99%

Vitamin A deficiency predisposes to Staphylococcus aureus infection

et al. 1996

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“…Liver biopsy samples were taken and used, together with the serum samples, for determination of retinol levels according to the method described by Catignani et al (9,25).…”

Section: Methodsmentioning

confidence: 99%

Increased translocation of Escherichia coli and development of arthritis in vitamin A-deficient rats

et al. 1995

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We studied the immune response and the colonization pattern in vitamin A-deficient rats that were colonized with the Escherichia coli O6 K13 pOmp 21 strain, which is genetically manipulated to produce ovalbumin and to be resistant to ampicillin. In the vitamin A-deficient rats, the number of bacteria per gram of feces was about five times higher than in the paired fed control rats 4 weeks after colonization. In the control rats, the colon and the lower part of the ileum were colonized, while in the vitamin A-deficient rats all parts of the small intestine, as well as the colon, were heavily inhabited by bacteria. Furthermore, in 75% of the vitamin A-deficient rats, the E. coli bacteria were found in the mesenteric lymph nodes, and in 50% of the rats E. coli were found in the kidneys. These animals also developed severe arthritis. The levels of serum immunoglobulin G (IgG), IgM, IgE, and biliary IgA antibodies against the bacterial antigens were significantly higher in the vitamin A-deficient rats than in the control rats. The number of IgA-producing cells in the lamina propria of the small intestine was significantly lower in the vitamin A-deficient rats than in the control rats; however, there was an increase in the number of CD8 ؉ cells and transforming growth factor ␤-producing cells in the lamina propria of the vitamin A-deficient rats. Disturbances in T-cell function were demonstrated, since spleen cells from the vitamin A-deficient rats produced more gamma interferon and interleukin-2 in vitro than control spleen cells. In summary, vitamin A deficiency led to a decrease in the ability to control the localization of intestinal bacteria and an increase in translocation, which was followed by development of arthritis regardless of substantial levels of antibacterial antibodies. The bacterial invasion made the animals hyperresponsive to the bacterial antigens, despite the fact that vitamin A deficiency is normally associated with suppressed antibody production, as previously shown by us and others.

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“…The vitamin A concentrations of the thawed plasma samples were determined fluorometrically by the method of Kahan (1966) using the modification to extraction suggested by Thompson et al (1971). Liver vitamin A concentration was determined by direct solvent extraction (Hinds et al, 1968) with acetone: petroleum ether (1:1) followed by spectrophotometric measurement using trichloroacetic acid as the chromogenic agent (Bayfield, 1971).…”

Section: Analytical Proceduresmentioning

confidence: 99%

Energy and nitrogen metabolism of diseased chickens: Interaction ofAscaridia galliinfestation and vitamin a status

Walker

Farrell

1976

British Poultry Science

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1. Effects of Ascaridia galli infection on the energy and nitrogen (N) metabolism were studied on groups of 5 cross-bred cockerels aged about 5 weeks and given a diet deficient or adequate in vitamin A at two levels of feeding in respiration chambers. 2. Metabolisability of dietary energy was 67% and N retention 33% in infected chickens compared with 71 and 41% respectively, in uninfected chickens. 3. Maintenance energy requirement of vitamin A-deficient birds was 882 kJ/kgW d compared with 998 kJ/kgW d for normal birds. N balance of the deficient chickens was also less when compared at the same energy balance. Infection did not affect maintenance energy requirement nor N balance. 4. Starvation heat production of infected chickens (619 kJ/kgW d) was higher than that of uninfected controls (586 kJ/kgW d). When infection treatments were combined, vitamin A-adequate chickens had a higher heat production (615 kJ/kg d) than the vitamin A-deficient (580 kJ/kgW d). Endogenous N excretion (mg/gW) was less in vitamin A-deficient than in adequate, starved birds. 5. Deficient chickens had undetectable liver reserves of vitamin A and only very low plasma concentrations. There was a difference in the length of larvae (17 d after infection) associated with vitamin A status, and with level of feeding.

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Methods of Extracting Vitamin A from Liver

Cited by 12 publications

References 0 publications

Vitamin A deficiency predisposes to Staphylococcus aureus infection

Vitamin A deficiency predisposes to Staphylococcus aureus infection

Increased translocation of Escherichia coli and development of arthritis in vitamin A-deficient rats

Energy and nitrogen metabolism of diseased chickens: Interaction ofAscaridia galliinfestation and vitamin a status

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