Mead acid supplementation does not rescue rats from cataract and retinal degeneration induced by N-methyl-N-nitrosourea

Fatty acids and their derivatives play a role in the response to ocular disease. Our current study investigated the effects of dietary mead acid (MA, 5,8,11-eicosatrienoic acid) supplementation on N-methyl-N-nitrosourea (MNU)-induced cataract and retinal degeneration in Sprague-Dawley rats. Experiment 1 was designed to inhibit cataract formation, with the dams fed a 2.4% MA or basal (<0.01% MA) diet during lactational periods. On postnatal day 7, male pups received a single intraperitoneal (ip) injection of 50 mg/kg MNU or vehicle. Lens opacity and morphology were examined 7 and 14 days after the MNU injection. Experiment 2 was designed to inhibit retinal degeneration and was performed with female postweaning rats. In this experiment, dams were fed the 2.4% MA or basal diet during the lactational periods. Thereafter, the female pups were continuously fed the same diets during their postweaning periods. On postnatal day 21 (at weaning), pups received a single ip injection of 50 mg/kg MNU. Retinal morphology was examined 7 days after the MNU injection. In experiment 3, six-week-old female rats were fed the 2.4% MA or basal diet starting at one week before the MNU injection and were then continuously fed the same diets until sacrifice. Rats at 7 weeks of age were given a single ip injection of 40 mg/kg MNU, and the retina was then examined morphologically one week after the MNU injection. In experiment 1, mature cataract was found in all of the MNU-treated groups, with or without MA supplementation. In experiments 2 and 3, atrophy of both the peripheral and central outer retina occurred in all rats exposed to MNU, with or without MA supplementation, respectively. The severities of the cataracts and retinal atrophy in the rats were similar regardless of MA supplementation. Dietary mead acid, which is used as a substitute in essential fatty acid deficiency in the body, does not modify MNU-induced cataract and retinal degeneration in rat models.     

维生素E缺乏对鲤骨骼肌损伤的影响

本文旨在探讨VE缺乏对鲤骨骼肌损伤的形态学影响。在半纯合日粮中分别添加0、25、50和100 mg/kg的VE,投喂体重约60 g的鲤鱼20周。结果表明:鲤鱼摄入VE缺乏的饲料后,出现“瘦背症”、脊柱弯曲及以突眼、竖鳞和腹水为特征的渗出性素质样病变。病理剖解见体壁肌肉萎缩,特别是背部两侧肌肉萎缩变薄,其厚度仅为对照组的1/4~1/2,似刀刃状;体侧红肌纤维褪色变白,呈白肌肉外观。组织学变化主要表现为肌营养性不良,骨骼肌变性、坏死,淋巴细胞和单核细胞浸润,大量结缔组织增生,残存的肌纤维萎缩变细。超微结构上表现为骨骼肌细胞核膜间隙增宽,呈锯齿状,并发生局部或广泛性的断裂,核变形,电子密度降低;肌浆内糖原颗粒明显减少,线粒体肿胀,嵴断裂,甚至溶解呈空囊泡状,肌原纤维的横纹模糊不清或完全消失。结论:日粮中0、25和50 mg/kgVE水平会导致鲤出现VE缺乏症,其骨骼肌主要表现为变性、坏死、肌萎缩和炎症细胞浸润的肌营养性不良。     

The failure of selenium supplementation to prevent copper-induced liver damage in Fischer 344 rats.

This study evaluates the ability of selenium (Se) supplementation to prevent experimental copper (Cu)-induced hepatocellular damage. Weanling male Fischer 344 rats were randomly assigned to groups of 15, 3 groups (A,B,C) were fed Cu-loaded diets (containing 2000 microg/g copper, added as CuSO4) and different levels of Se (added as Na2SeO3 x 5H2O) as follows: A) Cu-loaded/Se adequate diet (0.4 microg/g Se, fed basis); B) Cu-loaded/Se-supplemented diet (2 microg/g Se); and C) Cu-loaded/Se-deficient diet (< 0.2 microg/g). Three additional groups (D,E,F) were fed diets containing adequate levels of Cu (14 microg/g Cu, fed basis) and different levels of Se as follows: D) Cu-adequate/Se-adequate diet; E) Cu-adequate/Se-supplemented diet (2 microg/g Se); and F) Cu-adequate/Se-deficient (< 0.2 microg/g) diet. After 4, 8, and 12 weeks on the experimental diets, liver samples were processed for histology, histochemistry, metal analysis, glutathione peroxidase (GSH-Px) measurement, and quantification of malondialdehyde (MDA). Morphologic changes characteristic of Cu-associated hepatitis, without an increase in hepatic MDA levels, were seen in all Cu-loaded rats in each sampling. Similar changes occurred in rats fed Se-adequate, Se-supplemented and Se-deficient diets. This study demonstrates that Fischer 344 rats fed 2000 microg/g Cu develop morphologic changes due to Cu toxicity without evidence of lipid peroxidation. Furthermore, Se supplementation does not result in protection against Cu-induced liver injury.     

The Effect of Lecithin Supplementation on the Biochemical Profile and Morphological Changes in the Liver of Rats Fed Different Animal Fats

Sixty-four Wistar rats were divided into 8 equal groups and kept for 36 days in individual boxes. Three of the groups were given full synthetic diets containing various animal fats: beef tallow, pork fat or fish oil. A control group was fed the diets without the fat. The other four groups were fed the same diets with lecithin supplementation. At the end of experiment, sections taken from the liver were stained with haematoxylin–eosin and Sudan III to indicate fat infiltration. Liver enzyme levels, total bilirubin, albumin and two products of lipd metabolism were measured in serum from all the animals. The addition of lecithin to the diets did not influence the level of enzymes in the serum except in rats fed the diet containing beef tallow. A relationship between the type of diet, lecithin supplementation and the total cholesterol concentration in serum was observed. The concentration of HDL-cholesterol was only influenced by lecithin supplementation and that of triglycerides by the type of fat in the diet. The addition of lecithin to the diet was associated with proliferation of Kupffer cells, and an increased number of binuclear cells. Fatty degeneration of hepatocytes was less pronounced in all groups following lecithin supplementation. Lecithin supplementation of the diet did not elicit any pathological lesions and may be considered as a hepatocyte protector. This favourable effect of lecithin was most marked in the group of rats fed the fish oil.     

Analyses of hemorrhagic diathesis in high-iron diet-fed rats

Iron overload has been well recognized to cause oxidant-mediated cellular/tissue injury; however, little is known about the effects of iron overload on the blood coagulation system. We encountered an unexpected bleeding tendency in rats fed a high-iron diet in a set of studies using iron-modified diets. In this study, we investigated the mechanism of hemorrhagic diathesis induced by dietary iron overload in rats. Six-week-old F344/DuCrlCrlj male rats were fed a standard (containing 0.02% iron) or a high-iron diet (containing 1% iron) for 6 weeks and were then sampled for hematological, blood biochemical, coagulation, and pathological examinations. Serum and liver iron levels increased in rats fed the high-iron diet (Fe group) and serum transferrin was almost saturated with iron. However, serum transaminase levels did not increase. Moreover, plasma prothrombin time and activated partial thromboplastin time were significantly prolonged, regardless of the presence of hemorrhage. The activity of clotting factors II and VII (vitamin K-dependent coagulation factors) decreased significantly, whereas that of factor VIII was unaltered. Blood platelet levels were not influenced by dietary iron overload, suggesting that the bleeding tendency in iron-overloaded rats is caused by secondary hemostasis impairment. In addition, hemorrhage was observed in multiple organs in rats fed diets containing more than 0.8% iron. Our results suggest that iron overload can increase the susceptibility of coagulation abnormalities caused by latent vitamin K insufficiency.     

Cataracts and optic nerve hypoplasia in turkey poults

Newly hatched commercial turkey poults culled because of grossly visible cataracts were studied. A total of 43 affected and 23 unaffected control poults at various ages were necropsied, and the ocular changes in affected poults were compared with those of aged-matched controls. Affected poults had consistent cataracts coupled with a marked depletion in retinal inner plexiform, ganglion cell, and optic nerve fiber layers, with a resultant reduction in the size of the optic nerves. Lesions were seen in 1-day-old poults. Lens changes included microphakia and lens fiber degeneration throughout the lens, with nuclear liquefaction. The depletion in the numbers of retinal ganglion cells did not appear to progress over several weeks time. The ganglion cell depletion was not uniform within the retina. The cause for these ocular changes is unknown.     

The influence of diet on Lawsonia intracellularis colonization in pigs upon experimental challenge

The objective of this investigation was to study if different feeding strategies influence experimental infections of pigs with Lawsonia intracellularis, the causative agent of proliferative enteropathy. In three sequential trials, a total of 144 weaned pigs were fed five different diets all made from a standard diet based on wheat and barley as carbohydrate source and soybean as protein source. The five diets were: a standard diet (fine ground and pelleted), the standard diet fed as fermented liquid feed, the standard diet added 1.8% formic acid, the standard diet added 2.4% lactic acid and a diet similar to the standard diet (made from the same ingredients), but fed coarse ground. Twenty-four pigs on each diet were orally inoculated with L. intracellularis and growth performance and faecal excretion of bacteria were monitored. Twenty-four pigs fed the standard diet were included as not experimentally infected controls. Pigs in the first two trials were sacrificed 4 weeks post-inoculation, whereas animals in the third trial were sacrificed after 5 weeks. Pigs in all experimentally infected groups excreted L. intracellularis. The fermented liquid diet delayed the excretion of L. intracellularis and furthermore, pigs fed the standard diet supplemented with lactic acid had limited pathological lesions when the intestines were examined 4 weeks after inoculation. The growth performance was reduced in pigs experimentally challenged with L. intracellularis, however the prevalence and severity of diarrhea was limited.     

Assessment of Alloxan-Induced Diabetic Rats as a Periodontal Disease Model Using a Selective Cyclooxygenase (COX)-2 Inhibitor

Several recent studies have reported that alloxan-treated rats with long-term hyperglycemia can develop naturally occurring periodontal disease (PD). Our previous studies detected dental caries in the same model. Therefore, these two lesions of different etiologies are expected to occur concurrently. In this study, we evaluated the use of diabetic rats as a PD model by employing a selective COX-2 inhibitor reported to be effective against PD. Six-week-old female F344 rats were divided into 3 groups: intact rats (control), alloxan-induced diabetic rats fed a standard diet (AL) and alloxan-induced diabetic rats fed a diet containing 0.01% etodolac (AL+Et). The animals were euthanized at 26 weeks of age, and their oral tissues were examined histopathologically. Gingivitis, marginal periodontitis and alveolar bone resorption were markedly enhanced along with dental caries in the AL group compared with the control group. However, the COX-2 inhibitor had no effect on periodontal inflammation in the AL+Et group. In addition, in the AL group, periodontitis was notably nonexistent around the normal molars, and gingivitis was scarcely worse than that in the control group. In the diabetic rats, the progression of periodontal inflammation was closely correlated with the severity of adjacent dental caries, and marginal periodontitis was frequently continuous with apical periodontitis. In conclusion, an alloxan-induced diabetic rat is not a model of PD but of dental caries. It is probable that in this model, hyperglycemia may enable crown caries to progress to apical periodontitis, while the associated inflammation may rostrally expand to surrounding periodontal tissue.     

Early onset of disk degeneration and spondylosis in sand rats (Psammomys obesus)

The sand rat is a desert animal which feeds mainly on salt bush, a shrub with a high salt content in its leaves. Sand rats have been used for the study of renal function, and since they may develop diabetes if kept on a laboratory diet without a supplement of salt bush, they have been used for investigation of diabetes-related disorders as well. Older diabetic and non-diabetic sand rats are prone to develop severe degeneration of the intervertebral disks, disk herniation, and subsequent hyperostotic spondylosis. This report is concerned with the relation of these processes to aging. The vertebral columns of 25 sand rats which were fed a standard laboratory diet and a supplement of salt bush ad libitum were examined. The sand rats ranged from 12 to 18 months of age. The vertebral columns were dissected, prepared for microscopic examination, and the findings were compared with those obtained previously in sand rats from 1 1/2 to 2 1/2 years of age. Both disk degeneration and spondylosis were comparable in course and frequency to the changes found in the older sand rats. It was concluded that factors other than age are involved in the pathogenesis of disk degeneration in the sand rat.     

Optic pathway degeneration in Japanese black cattle

Degeneration of the optic pathway has been reported in various animal species including cattle. We experienced a case of bilateral optic tract degeneration characterized by severe gliosis in a Japanese black cattle without any obvious visual defects. To evaluate the significance, pathological nature and pathogenesis of the lesions, we examined the optic pathway in 60 cattle (41 Japanese black, 13 Holstein and 6 crossbreed) with or without ocular abnormalities. None of these animals had optic canal stenosis. Degenerative changes with severe gliosis in the optic pathway, which includes the optic nerve, optic chiasm and optic tract, were only observed in 8 Japanese black cattle with or without ocular abnormalities. Furthermore, strong immunoreactivity of glial fibrillary acidic protein was observed in the retinal stratum opticum and ganglion cell layer in all 5 cattle in which the optic pathway lesions could be examined. As etiological research, we also examined whether the concentrations of vitamin A and vitamin B12 or bovine viral diarrhea virus (BVDV) infection was associated with optic pathway degeneration. However, our results suggested that the observed optic pathway degeneration was probably not caused by these factors. These facts indicate the presence of optic pathway degeneration characterized by severe gliosis that has never been reported in cattle without bilateral compressive lesions in the optic pathway or bilateral severe retinal atrophy.     

Semi‐synthetic diet versus diet using natural ingredients—Comparative study in female Golden Syrian hamsters

Semi‐synthetic diets (SSD) are recommended and are widely used to carry out experiments in rodents. However, in our experiments planned to carry out generation studies in female Golden Syrian hamsters using semi‐synthetic diets, it was observed that the hamsters did not conceive as a result of decreased food intake. In this paper, we present the effects of both semi‐synthetic diets and natural source diets (NSD) on food intake, body weight and reproductive performance of this species. Four‐week‐old female hamsters were equally divided into 3 groups and initially acclimatized for 2 weeks on natural chow diet (NCD). Thereafter, they were fed either control diet, high fat diet (HFD) or low protein diet (LPD) based on semi‐synthetic/natural source ingredients until 12 weeks. Daily food intake and weekly body weights were monitored. Hamsters were kept for mating for about 2 weeks from 10th week onwards, during which the pregnancy confirmation test was done using standard vaginal smear examination. In all the groups fed SSD, the food intake was very poor, hamsters lost body weight and did not conceive, thus preventing us from carrying out further experiments. Hamsters fed NCD/NSD ingested more than twice as much as hamsters fed SSD (7–8 g/day/hamster against 3 g/day/hamster on average respectively). Based on the results of the current research, we conclude that the routinely used semi‐synthetic diet is not suitable for carrying out studies in female hamsters. We suggest that scientists must also consider the unusual biological characteristics of a given species besides other biological factors. It is therefore critical to select appropriate biological models and diets that provide optimal sensitivity and specificity to accomplish the research objectives.     

Blindness in goats following ingestion of Stypandra glauca

Twenty-seven of 427 Angora goats of mixed age became blind within a week of consuming large amounts of Stypandra glauca ("nodding blue lily"). A further 200 goats were depressed for several weeks, but most subsequently recovered. Blindness was associated with optic nerve neuropathy which is postulated to have followed compression of the optic nerves within the bony optic canals as a result of severe myelin oedema. Histologically, the intracanalicular portion of the optic nerve was sclerotic, while the intracranial portion of the optic nerve and the optic tracts were degenerating. The retrobulbar portion of the optic nerve was relatively unaffected. In addition, multifocal retinal photoreceptor degeneration was found ophthalmoscopically and histologically. The syndrome was not reproduced during a trial in which 2 goats were fed 4 and 20 kg of S. glauca harvested after it had finished flowering, more than 3 weeks after the first natural cases of blindness. Based on epidemiological and pathological data we propose that S. glauca is toxic to stock, but only for a short period while flowering in spring.     

Amaurosis in sheep resulting from treatment with rafoxanide

Amarurosis occurred in sheep on various farms in the Republic of South Africa after treatment with rafoxamide. Histopathological examination revealed a status spongiosus of varying severity in the central nervous system in all the cases, having a predilection for certain areas such as the periventricular area of the lateral ventricles, optic tracts, lateral geniculates and optic fasiculi. The retina was the only ocular tissue affected and lesions observed in the retina included necrosis of nerve cells in the ganglionic layer. In chronic cases of amaurosis this layer showed a complete absence of nerve cells. The possible pathogenesis of the lesions and their differentiation from those found in certain plant toxicoses are discussed.     

Fat source affects growth of weanling rats fed high-fat diets low in zinc

In two 3-week experiments with a 2-factorial design, weanling rats were fed semi-purified diets in which the zinc concentration was either suboptimal or adequate for maximum growth. In experiment 1, one low-fat diet and four diets enriched with 26% beef tallow (BT), butterfat (BF), coconut oil or sunflower oil (SF) were compared. The low-Zn SF diet did not support growth. The animals fed the high-Zn SF diet had the lowest final weights among all other groups, and their serum and femur Zn concentrations were markedly depressed. In experiment 2, the low- and high-Zn diets were enriched with 18% BT, SF, BT + SF (1:1 w/w), or olive oil (OL). Final live weights showed a Zn × fat source interaction. The low-Zn SF and OL groups consumed less food and weighed less than the low-Zn BT group. At the high-Zn level, final weights were comparable among groups. Serum and femur Zn concentrations did not significantly vary among groups fed diets with the same Zn level. Possibilities for the growth-retarding effect of the diets rich in unsaturated fatty acids (SF and OL) are discussed. Metabolic studies are needed to clarify the observed zinc × fat source interaction.     

Morphological and biochemical assessment of the liver response to excess dietary copper in Fischer 344 rats.

The aim of this study was to determine the amount of excess dietary copper (Cu) necessary to experimentally induce liver lesions characteristic of Cu-associated disease in Fischer 344 rats. Male weanling Fischer 344 rats of uniform age were divided into 6 groups (n = 5) and fed a rodent diet containing 18 (control), 750, 1000, 1250, 1500, and 2000 microg/g Cu added as CuSO4. Rats were euthanized after 3 months on the experimental diets and their livers processed for histology, histochemistry, Cu analysis (by atomic absorption spectrophotometry), and quantification of malondialdehyde (MDA) by the thiobarbituric acid reaction. Hepatic Cu levels were significantly higher (P < 0.01) in rats receiving over 1000 microg/g Cu compared to the controls (means for each diet: control = 4.8 microg/g, 750 microg/g Cu = 39.6 microg/g, 1000 microg/g Cu = 111.2 microg/g, 1250 microg/g Cu = 389 microg/g, 1500 microg/g Cu = 509.4 microg/g, and 2000 microg/g Cu = 766 microg/g). Histological lesions increased gradually according to the level of dietary Cu. Significant morphologic changes (necrosis, portal inflammation, hyaline remnants) and reduced growth rate occurred in rats receiving over 1250 microg/g Cu. However, no significant differences were found for MDA levels between groups. The present study demonstrates that compared to other species, very high levels of excess dietary Cu are needed to induce significant liver injury in Fischer 344 rats. Increased MDA content was not detected in rats with morphologic evidence of liver damage, suggesting that lipid peroxidation may not play a major role in this model of Cu toxicity.     

Influence of diet on the experimental infection of pigs with Brachyspira pilosicoli

The effects of five different diets on the experimental infection of pigs with a Danish field isolate of Brachyspira pilosicoli were investigated. The diets tested were a pelleted and a non-pelleted standard diet based on wheat and barley, the standard diet supplemented with 2 per cent lactic acid, a fermented liquid feed and a diet based on cooked rice. Two trials were conducted, each with six groups of six pigs; in each, two of the groups were fed the standard diet. One of these groups and the other four groups were challenged after two weeks on the diets and euthanased four weeks later. The clinical signs of B pilosicoli infection varied from loose stools to watery, mucoid diarrhoea. The group fed the rice diet excreted B pilosicoli in their faeces for a significantly shorter period than the group fed the standard diet (P < 0.01), and fewer of them excreted the organism (P < 0.05). All the pigs fed the pelleted diet excreted B pilosicoli in their faeces, and significantly more of them showed clinical signs of disease than the pigs fed the standard diet (P < 0.05). The fermented liquid feed and the diet containing lactic acid had no significant effect on the excretion of B pilosicoli or on the numbers of pigs showing clinical signs of disease.     

Distinctive histopathologic features of canine optic nerve hypoplasia and aplasia: a retrospective review of 13 cases

Canine optic nerve hypoplasia (ONH) and aplasia (ONA) are significant neuro-ophthalmologic disorders that have been reported in several species. The purpose of this study was to describe the distinctive histopathologic features of ONH and ONA in canine patients identified from a collection of 20 000 ocular submissions at the comparative ocular pathology laboratory of Wisconsin from 1989 to 2006. The following information about ONH and ONA cases was collected: signalment, and clinical and gross findings, including unilateral vs. bilateral involvement. Microscopic evaluation was performed, with attention to optic nerve malformation, retinal ganglion cell (RGC) and nerve fiber layer (NFL) loss, and retinal disorganization. The distribution of retinal vasculature was recorded and a search for unusual findings of ONH and ONA was performed. Information and histologic documentation was available for 13 cases. Eight cases of ONH and five cases of ONA were identified. The average group age was 20.2 months and 16.1 months, respectively. The most common breed was the Shih Tzu (3/13). ONH usually presented bilaterally (7/8); all ONA cases presented as a unilateral disease (5/5). The morphologic findings in the optic nerve (ON) in ONH included variable degrees of ON hypoplasia and gliosis, as well as ectopic vestigial ON remnants within orbital nerves and connective tissues. The NFL was detected in the majority of the ONH cases; however, RGCs were rare or absent. Mild retinal disorganization was seen occasionally. Most cases of ONH were associated with regional peripheral retinal blood vessel extension into the vitreous, leaving the peripheral retina avascular. In ONA cases the retinal blood vessels, NFL and RGCs were totally absent and retinal disorganization was severe. Distinctive microscopic features encountered in ONA included anterior segment dysgenesis in some cases. The retina in these cases was stretched across the posterior lens capsule, never making contact with the posterior pole of the globe. The current study reviews the human and veterinary literature pertaining to ONH and ONA, compares ONH and ONA in dogs, and presents related ophthalmic histopathologic findings that have not been reported previously.     

Effect of dietary protein,essential and non‐essential amino acids on the performance and carcase composition of male broiler chickens

1. The present study was conducted to determine the possibility of using low‐protein broiler diets supplemented with synthetic amino acids. The effects on performance, carcase composition and nitrogen retention were evaluated.)

2. A starter diet was given, ad libitum, from 7 to 21 and a finisher diet from 21 to 42 d of age. Body weight, weight gain, food intake and food conversion (FC) were determined at 3 and 6 weeks of age. Abdominal fat deposition (AFD), carcase yield, carcase fat and protein and nitrogen retention were determined at 6 weeks of age. During the starter period chicks were given a 231 g/kg crude protein (CP) diet and a low protein diet supplemented with synthetic amino acid, a: to National Research Council recommendations, b: to the concentration of the control diet, and c: in agreement with the pattern of body composition. Glutamic acid and glycine were added to some diets as sources of non‐essential amino acids (NEAA). All diets contained 12.62 MJ metabolisable energy (AME_n)/kg. The diets administered between 3 and 6 weeks were comparable to the starter diets, except that they contained more AME_n (12.85 MJ/kg) and less protein.

3. Performance equal to that of high protein controls was obtained with birds fed a low protein diet supplemented with synthetic essential and NEAA to the amounts in the control diet or based on the amino acid profile of body protein. This was not achieved with low protein diets supplemented with synthetic amino acids to the amounts recommended by NRC.

4. Without altering performances, the efficiency of protein utilisation of birds fed on low protein diets was superior to that of birds fed on the commercial control diet and their nitrogen excretion was reduced by 26%. The percentage carcase yield and protein was unaffected by the dietary regimen but carcase fat content and AFD increased as the protein content of the diet decreased.

5. These results show that it is possible to obtain the same performances with low protein diets supplemented with synthetic amino acids, using an ideal amino acid balance. However, low protein diets result in a higher carcase fat content.     

Influence of variable content of dietary zinc on copper metabolism of weanling foals

The influence of variable zinc content (29.1, 250, 1,000 and 2,000 mg/kg of dry weight) in a basic diet containing 7.7 mg of copper/kg on the ability of weanling foals to maintain normal copper balance was investigated. Serum copper and zinc concentrations were monitored, and terminal hepatic copper and zinc contents were measured in 4 weanling foals fed the basic diet containing 29.1 mg of zinc/kg and in 2 foals each fed the higher-zinc diets. Foals fed the lower-zinc diets (29.1 and 250 mg/kg) maintained normal serum copper and zinc concentrations for 14 to 15 weeks, whereas those fed the 2 higher-zinc diets became hypocupremic within 5 to 6 weeks and were lame within 6 weeks, owing to cartilaginous disease characteristic of osteochondritis dissecans. Serum zinc concentration in the foals fed the 2 higher-zinc diets increased to greater than 2 micrograms/ml within 2 weeks. Foals fed the high-zinc diets became lame after serum copper concentration had remained at 0.3 micrograms/ml for greater than 1 week. Serum copper concentration in these arthritic foals was less than or equal to 0.2 micrograms/ml at the end of the study. In lame foals, fractures of the cartilage of the articular and growth physes occurred through the zone of hypertrophic cells, and varied from bilateral to unilateral and from small to large. Free masses and flaps of cartilage attached to one side were numerous.     

Ultrastructural alterations of the myocardium of rats fed rapeseed oils.

Ultrastructural studies were conducted on the myocardium of rats fed corn oil, Tower RSO (0 . 88 per cent EA), 1788 RSO (3 . 6 per cent EA) and Target RSO (38 . 9 per cent EA) supplemented diets for 18 weeks. Cardiac myocytes of Tower RSO-fed rats showed some loosening of myofibrils and a slight increase in the number of mitochondria, few of which had lost their cristae. Large intravascular lipid droplets were observed in the myocardium of rats fed the 1788 RSO diet, as well as some small lipid droplets which were seen in close association with mitochondria. There was an apparent increase in the number of mitochondria of both normal and giant size. Many of the mitochondria exhibited distortion of shape and degeneration of cristae. The matrix of megamitochondria contained vesicles and electron-dense floccular inclusions and at times electron-lucent lipid-like material. The degenerative changes of mitochondria were most pronounced in the Target RSO group, where some megamitochondria showed a complete loss of cristae and a replacement of matrix with lipid-like material. These observations suggest that both intravascular lipid globules and the mitochondrial alterations are possible contributory factors involved in the development of cardiac lesions in RSO-fed rats.