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Evidence of multiple metabolic routes in vanadium's effects on layers. Ascorbic acid differential effects on prepeak egg production parameters following prolonged vanadium feeding.

作者信息

Toussant M J, Latshaw J D

机构信息

Department of Poultry Science, Ohio State University, Columbus 43210.

出版信息

Poult Sci. 1994 Oct;73(10):1572-80. doi: 10.3382/ps.0731572.

Abstract

The development of V toxicity was followed over a 28-d period in 25-wk-old Leghorn layers fed 20 mg ammonium metavanadate/kg diet (Days 1 to 14) followed by 30 mg/kg diet (Days 15 to 28). Then, over a second 28-d period, the responses to V and supplemental ascorbic acid (AA) fed at 500 or 1,000 mg/kg diet (Days 29 to 42) followed by 1,500 or 3,000 mg/kg diet (Days 43 to 56) were examined. Feed consumption, egg weight, Haugh units (HU), and BW measurements indicated that the response to V was multifactorial, but of differing intensities and time-frames for the variables. Haugh units were lowered rapidly (3 d, P < .05) in response to V feeding, but HU values decreased only slightly when dietary V was increased to 30 mg/kg. In contrast, egg production was decreased moderately by 20 mg V/kg and a considerable further reduction in egg production resulted from increasing the V to 30 mg/kg. Ascorbic acid supplementation differentially affected these responses: BW, egg production, and egg weight were improved significantly in the V-fed group receiving an AA supplement, as compared with those fed V only. Haugh unit values, however, were not improved by AA supplementation in groups receiving V. Foam functional properties, which also were changed by V feeding, were not corrected by AA feeding. The results suggest that the toxic effects of V are mediated through more than one physiological mechanism. One mechanism, which includes negative effects on BW, egg production, and egg weight, is responsive to the additional reducing equivalents provided by supplemental AA. Another mechanism, which is apparent from the effect of V on egg HU values, is not ameliorated by AA supplementation after toxicity developed.

摘要

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