Vascular changes and liver tumours induced in mink by high levels of nitrite in feed.

Two groups of female mink were fed a diet supplemented with 30-50 mg/kg bw sodium nitrite for up to six years. The first group also received dimethylamine hydrochloride. Seven male offspring from litters born in the first year were fed the same diet for nine months but showed no pathomorphological change. After three years on trial, female mink developed occlusive changes in some branches of the efferent hepatic veins, and 21% of the mink in group 1 and 31% in group 2 developed liver haemangioendotheliomas or precancerous liver changes. The pathomorphological changes were identical to those seen in animals exposed to N-nitrosodimethylamine (NDMA). This result indicates in-vivo formation of NDMA as a result of the high nitrite in the diet. However, NDMA was not measured in the blood of the nitrite-exposed mink.

Embryonic death in mink due to riboflavin deficiency.

Riboflavin deficiency has been produced experimentally in mink by adding to the feed 10--20 mg galactoflavin--anti-B2 vitamin--per animal daily during the pregnancy. The experiment included 44 standard female mink (Table II). Riboflavin deficiency led to embryonic death; none of the mated females in the deficient group delivered kits. At the expected time of birth, six of the females were subjected to uterectomy or investigative laparatomy, which showed remnants of embryos that were mostly decomposed (Figs. 1 and 2). In a parallel group, four of six females on the same diet with the same doses of galactoflavin, but with 50--100 mg riboflavin added daily, delivered normal litters (Table II). Five standard male mink were placed on the same experimental diet supplemented with 30 mg galactoflavin per animal daily from 15/12 to 18/3. The fertility of these males was not influenced in a negative way.

Hypervitaminosis D in fur-bearing animals.

Investigations concerning the effect on fur-bearing animals of large doses of vitamin D3 were carried out. The material comprised 62 animals in all--10 silver foxes, 17 blue foxes and 35 mink (Table II). Daily doses of 5 IU vitamin D3/g body weight for two months did not produce clinical symptoms in the foxes. However, a short while after the dose was increased to 10 IU, the animals showed loss of appetite, had difficulty in moving, were apathetic and developed dark coloured faeces. Analysis of blood serum showed markedly raised calcium values (Table III). Calcium deposits were demonstrated in the kidneys and in some cases also in the musculature, gastric mucosa, bronchi and the larger blood vessels. No abnormal signs were shown by 30 mink which received 0.6--0.7 IU vitamin D3/g body weight for five months. PM findings were normal.

[The formaldehyde content in fish in relation to anemia in mink (author's transl)]. / Formaldehydinnholdet i fisk i relasjon til anemi hos mink

The fish-induced anemia in mink is an alimentary disease produced by feeding high amounts of some raw marine fishes. The anemiogenic properties of the fish has been related mainly to its content of the iron binding agent-trimethylaminoxide. The aim of the present investigation was to examine how far formaldehyde could also play a part as an anemiogenic factor. The content of formaldehyde has been analysed in all species of raw, cold stored fish known to be used in mink food and in a few samples of ready made food (Table II). The content of formaldehyde varied within wide limits from 12 to 105 ppm, but none of the measured contents reached the high values obtained by Costly (1970). The mean values of formaldehyde in gutted coalfish, fillet waste of coal fish, cod and haddock prepared for the feeding experiments, were all close to 50 ppm. 175 female mink and 632 mits were tested during the whole of the breeding period from 15.2-30.6, 80 per cent of the diet (page 1) was fish products with and without supplements of formaldehyde. Amounts from 200 to 50 ppm were tried (Table I). The supplement of 200 ppm formaldehyde had an appetite-decreasing and anemiogenic effect, but the supplement of 50 ppm, i.e. a formaldehyde content up to the highest value observed in fillet waste, had no effect on appetite or hemoglobin synthesis neither in females nor in kits. This content of formaldehyde did not counteract the anti-anemiogenic effect of iron glutamate. The fish-induced anemia occurred in mink thus appears unaffected by the quantities of formaldehyde found in fish diets to fur bearing animals. Triox must be regarded as the dominant anemiogenic factor in raw fish diets.