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  • Author or Editor: Hidetoshi Higuchi x
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Abstract

Objective—To evaluate serum lipid peroxide (LPO) and α-tocopherol concentrations and superoxide dismutase (SOD) activity in captive bottle-nosed dolphins and to evaluate effects of storage on production of LPO in various marine fish.

Animals—16 bottle-nosed dolphins.

Procedure—8 dolphins (group A) were fed chub mackerel and herring (high fat) and arabesque greenling and banded blue-sprat (low fat); the other 8 dolphins (group B) were fed chub mackerel and Pacific saury (high fat) and shishamo smelt and Japanese horse mackerel (low fat). Each group had been on these respective diets for 3 years. Serum LPO and α-tocopherol concentrations, serum SOD activity, and superoxide production by neutrophils were measured. All types of marine fish were frozen at –20 C for 6 months, and concentrations of LPO were measured at various time points.

Results—Serum LPO concentrations in group-A dolphins were significantly higher than those in group B. Serum α-tocopherol concentrations and SOD activity in group A were significantly lower than those in group B. A significant negative correlation was found between serum LPO and α-tocopherol concentrations in all 16 dolphins. The LPO concentrations in mackerel and herring fed to group-A dolphins were higher than those of other fish. Concentrations of LPO in herring stored for 3 and 6 months at –20 C were higher than those in herring before freezing and in herring stored for 1 month.

Conclusions and Clinical Relevance—Serum LPO and α-tocopherol concentrations in captive bottlenosed dolphins may be strongly influenced by high amounts of polyunsaturated fatty acid and LPO found in marine fatty fishes. High concentrations of serum LPO, as found in group-A dolphins, were associated with decreased antioxidative states. Monitoring of serum LPO and α-tocopherol concentrations and serum SOD activity may be useful for the management of captive marine mammals. (Am J Vet Res 2001;62:1952–1956)

Full access
in American Journal of Veterinary Research

Summary

Parenchymal cells were isolated from the liver of male calves, and monolayer cultures formed were treated with glucocorticoids to examine whether haptoglobin, appearance of which is associated with hepatic lipidosis (fatty liver) in cattle, is induced by steroid hormones. Without addition of dexamethasone, only trace amounts of haptoglobin were detected in culture medium. With addition of dexamethasone (10−12 to 10−4 M), considerable amounts of haptoglobin were released into the medium. Maximal release was observed at concentrations of 10−8 to 10−6 M dexamethasone. Haptoglobin release was similarly induced by Cortisol, although the effect was less potent than that of dexamethasone. Actinomycin D (a known protein synthesis inhibitor) dose-dependently reduced amounts of haptoglobin released in response to 10−8 M dexamethasone. Dexamethazone also induced annexin I, which is known to be synthesized in response to glucocorticoids. Dexamethasone treatment resulted in reduced protein kinase C activity in the cell cytosol, which has been shown to be an early event in dexamethasone-treated cells. Other than glucocorticoids, estradiol induced haptoglobin release, whereas progesterone was less effective. The association of haptoglobin with hepatic lipidosis can be reasonably explained by the fact that haptoglobin production by the liver is induced by glucocorticoids and estradiol, and these steroid hormones are triggers for development of hepatic lipidosis in cattle.

Free access
in American Journal of Veterinary Research