Safety of 25-hydroxyvitamin D3 as a source of vitamin D3 in layer poultry feed.

A target animal safety study investigated the effects of providing 25-hydroxyvitamin D3 (25-OH-D3) in laying hen feed at levels ranging from 0.5 to 10 times the level commonly used for vitamin D3 supplementation in the poultry industry. Following a 28-day preconditioning period, 5 groups of laying hens were fed commercial diets containing 68.9 micrograms of vitamin D3/kg feed (control) or 41.25 (0.5x), 82.5 (1x), 412.5 (5x), or 825 (10x) micrograms of 25-OH-D3/kg feed. The study compared the effects of the control level of vitamin D3 and the various test levels of 25-OH-D3 on health, performance, hematology, and 25-OH-D3 tissue concentrations in laying hens from 0 to 112 d of treatment and on health, performance, gross pathology and histopathology from 113 to 224 d of treatment. Gross pathologic and histopathologic examination of selected tissues after 224 d revealed no lesions attributable to vitamin D toxicity at any level of test material. Concentrations of 25-OH-D3 in edible tissues at 112 d were similar for birds in the control and 1x groups. On the basis of all variables monitored, including body weight gain and feed conversion, the 10x level of 25-OH-D3 produced clear toxicity (but no mortality), the 5x level caused limited threshold toxicity, and the 1x level induced no toxicity. These results indicate that 25-OH-D3 is safe for use in laying hen feed as a source of vitamin D3 at 82.5 micrograms/kg feed (1x), with a margin of safety of approximately 5x between the proposed 1x level and the 5x level (412.5 micrograms/kg feed) that constitutes threshold toxicity in layers.

Safety of 25-hydroxyvitamin D3 as a source of vitamin D3 in turkey rations.

A target animal safety study investigated the effects of providing 25-hydroxyvitamin D3 (25-OH-D3) as a replacement for vitamin D3 in pelleted turkey feeds. Five groups of turkeys were fed diets containing vitamin D3 at 68.9 micrograms/kg feed (control) or 25-OH-D3 at concentrations of 49.5 (0.5x), 99 (1x), 495 (5x) or 990 (10x) micrograms 25-OH-D3/kg feed. The effects of 25-OH-D3 or vitamin D3 on performance, health, hematology, gross pathology and tissue concentrations of 25-OH-D3 in female and male turkeys were compared at 112 days of feeding. There was no significant difference from control in pen body weight in any of the groups. When feed conversion was calculated without taking into account body weights of birds that died during the study, there was no significant difference from control in any of the groups. When feed conversion was corrected for mortality, the only significant effect was that females at the 5x level (495 micrograms 25-OH-D3/kg feed) had improved feed conversion. Significantly increased mortality occurred during the study in the 10x (990 micrograms 25-OH-D3/kg feed) male group only. No histomorphologic tissue alterations attributable to dietary administration of 25-OH-D3 were observed in tissues examined at any dietary level of 25-OH-D3. 25-OH-D3 did not adversely affect animal health at the proposed use level of 99 micrograms/kg feed when replacing vitamin D3 in turkey rations. The proposed use level also provides at least a 5-fold margin of safety.

Bacterial metabolism of arylsulfonates: role of meta cleavage in benzene sulfonate oxidation by Pseudomonas testosteroni.

Pseudomonas testosteroni H-8 oxidizes certain lower alkylbenzene sulfonates at rates inversely related to the length of the alkyl group. Appreciable Q(O)2 values were observed for benzene sulfonate (BS), toluene sulfonate (TS), and ethylbenzene sulfonate (EBS), but not for propylbenzene sulfonate (PS) and higher homologues. Catechol oxidation was catalyzed by a constitutive catechol-2,3-oxygenase (EC 1.99.2.a). Yellow meta cleavage products accumulated when BS-grown cells were exposed to catechol, 4-methylcatechol, 3-methylcatechol, EBS and PS, but not BS or TS. Traces of a yellow metabolite (probably 2-hydroxymuconic semialdehyde) were detectable during growth on BS. PS completely inhibited growth on BS, but not on L-leucine or nutrient broth. Also, PS antagonized respiration on BS and catechol, but not glutamate, the extent of inhibition being directly related to PS concentration. Formation of a meta cleavage product from PS, and inhibition of catechol oxidation by PS, suggested that the actual inhibitor may not be PS itself, but a metabolite.