Lynn F. James

Effects of poisonous plants on livestock

Effects of poisonous plants on livestock , Effects of poisonous plants on livestock , مرکز فناوری اطلاعات و اطلاع رسانی کشاورزی

Chemistry of toxic range plants. Highly oxygenated flavonol methyl ethers from Gutierrezia microcephala

Abstract The perennial American desert shrub, Gutierrezia microcephala, contains 20 flavonol methyl ethers displaying nine different oxygenation patterns. These include 11 new flavonols: 5,7-dihydroxy-3,6,8,3′,4′,5′-hexamethoxyflavone, 5,7,4′-trihydroxy-3,6,8,3′,5′-pentamethoxyflavone, 5,7,3′-trihydroxy-3,6,8,4′,5′-pentamethoxyflavone, 5,7,2′,4′-tetrahydroxy-3,6,8,5′-tetramethoxyflavone, 5,7,3′,4′-tetrahydroxy-3,6,8-trimethoxyflavone, 5,7,8,3′,4′-pentahydroxy-3,6-dimethoxyflavone, 3,5,7,3′,4′-pentahydroxy-6,8-dimethoxyflavone, 5,7,4′-trihydroxy-3,6,8-trimethoxyflavone, 5,7,8,4′-tetrahydroxy-3,3′-dimethoxyflavone, 5,7,8,3′,4′-pentahydroxy-3-methoxyflavone and 5,7,8,4′-tetrahydroxy-3-methoxyflavone. In addition, the following known flavonols were isolated: 5,7-dihydroxy-3,8,3′,4′,5′-pentamethoxyflavone, 5,7,4′-trihydroxy-3,8-dimethoxyflavone, 5,7,4′-trihydroxy-3,8,3′-trimethoxyflavone, 5,7,3′,4′-tetrahydroxy-3,8-dimethoxyflavone, 5,7,4′-trihydroxy-3,6,3′-trimethoxyflavone, 5,7,3′,4′-tetrahydroxy-3-methoxyflavone, 5,4′-dihydroxy-3,6,7,8,3′-pentamethoxyflavone, 5,7,4′-trihydroxy-3,6,8,3′-tetramethoxyflavone and 3,5,7,4′-tetrahydroxy-6,8,3′-trimethoxyflavone.

The Lesions of Locoweed (Astragalus mollissimus), Swainsonine, and Castanospermine in Rats

To better characterize and compare the toxicity of and lesions produced by locoweed (Astragalus mollissimus) with those of swainsonine and a related glycoside inhibitor, castanospermine, 55 Sprague-Dawley rats were randomly divided into 11 groups of five animals each. The first eight groups were dosed via subcutaneous osmotic minipumps with swainsonine at 0,0.1,0.7,3.0,7.4, or 14.9 mg/kg/day or with castanospermine at 12.4 or 143.6 mg/kg/day for 28 days. The last three groups were fed alfalfa or locoweed pellets with swainsonine doses of 0, 0.9, or 7.2 mg/kg/day for 28 days. Swainsonine- and locoweed-treated rats gained less weight, ate less, and showed more signs of nervousness than did controls. Histologically, these animals developed vacuolar degeneration of the renal tubular epithelium, the thyroid follicular cells, and the macrophage-phagocytic cells of the lymph nodes, spleen, lung, liver, and thymus. Some rats also developed vacuolation of neurons, ependyma, adrenal cortex, exocrine pancreas, myocardial epicytes, interstitial cells, and gastric parietal cells. No differences in lesion severity or distribution were detected between animals dosed with swainsonine and those dosed with locoweed. Rats dosed with castanospermine were clinically normal; however, they developed mild vacuolation of the renal tubular epithelium, the thyroid follicular epithelium, hepatocytes, and skeletal myocytes. Special stains and lectin histochemical evaluation showed that swainsonine- and castanospermine-induced vacuoles contained mannose-rich oligosaccharides. Castanospermine-induced vacuoles also contained glycogen. These results suggest that 1) swainsonine causes lesions similar to those caused by locoweed and is probably the primary locoweed toxin; 2) castanospermine at high doses causes vacuolar changes in the kidney and thyroid gland; and 3) castanospermine intoxication results in degenerative vacuolation of hepatocytes and skeletal myocytes, similar to genetic glycogenosis.

Comparative Toxicosis of Sodium Selenite and Selenomethionine in Lambs

Excess consumption of selenium (Se) accumulator plants can result in selenium intoxication. The objective of the study reported here was to compare the acute toxicosis caused by organic selenium (selenomethionine) found in plants with that caused by the supplemental, inorganic form of selenium (sodium selenite). Lambs were orally administered a single dose of selenium as either sodium selenite or selenomethionine and were monitored for 7 days, after which they were euthanized and necropsied. Twelve randomly assigned treatment groups consisted of animals given 0, 1, 2, 3, or 4 mg of Se/kg of body weight as sodium selenite, or 0, 1, 2, 3, 4, 6, or 8 mg of Se/kg as selenomethionine. Sodium selenite at dosages of 2, 3, and 4 mg/kg, as well as selenomethionine at dosages of 4, 6, and 8 mg/kg resulted in tachypnea and/or respiratory distress following minimal exercise. Severity and time to recovery varied, and were dose dependent. Major histopathologic findings in animals of the high-dose groups included multifocal myocardial necrosis and pulmonary alveolar vasculitis with pulmonary edema and hemorrhage. Analysis of liver, kidney cortex, heart, blood, and serum revealed linear, dose-dependent increases in selenium concentration. However, tissue selenium concentration in selenomethionine-treated lambs were significantly greater than that in lambs treated with equivalent doses of sodium selenite. To estimate the oxidative effects of these selenium compounds in vivo, liver vitamin E concentration also was measured. Sodium selenite, but not selenomethionine administration resulted in decreased liver vitamin E concentration. Results of this study indicate that the chemical form of the ingested Se must be known to adequately interpret tissue, blood, and serum Se concentrations.

Social facilitation influences cattle to graze locoweed.

Many ranchers claim that if a cow starts eating locoweed, she will teach others to eat it. Three grazing trials were conducted to evaluate the role of social facilitation in starting cattle to graze locoweed. The first trial was conducted near Gladstone, N.M., using mature cows grazing woolly locoweed (Astragalus mollissimus var. mollissimus Torr). The second trial was conducted on the Raft River Mountains in northwestern Utah, using yearling cattle grazing white locoweed (Oxytropis sericea Nutt). The third trial was conducted to determine if aversion-conditioned yearling cattle would consume white locoweed when placed with cattle that were eating locoweed (loco-eaters). Cattle conditioned to eat locoweed and naive animals in trials 1 and 2 first grazed in separate pastures to evaluate their initial acceptance of locoweed. The groups in the respective trials then were placed together to evaluate the influence of social facilitation on locoweed consumption. Locoweed consumption was quantified by bite count. Naive cattle in trials 1 and 2 sampled small quantities of locoweed while grazing separately. However, they greatly increased locoweed consumption when placed with the loco-eaters. Aversion-conditioned cattle in trial 3 did not consume locoweed while grazing separately. When placed with loco-eaters, they gradually increased consumption of white locoweed, in contrast to the immediate acceptance of locoweed by naive cattle in trials 1 and 2. The aversion extinguished and averted animals eventually accepted white locoweed at levels comparable to loco-eaters. Results of this study demonstrate that social facilitation can cause cattle to start eating locoweed.

Comparative Pathology of Astragalus (Locoweed) and Swainsona Poisoning in Sheep

The toxic effect on pregnant two of Swainsona galegifolia (collected in Australia) and of Astragalus pubentissimus and A. Ientiginosus (collected in the United States) were compared. The signs of intoxication, vacuolar lesions, and clinicopathologic changes were similar. These similarities suggest that the toxic agent or agents may be the same in both genera. Some sheep fed Astragalus aborted and some delivered deformed lambs while those fed Swainsona did not.

Pathology of Locoweed Poisoning in Sheep

Three locoweeds, Oxytropis sericea, Astragalus pubentissimus, and A. lentigimosus were fed experimentally to yearling wethers for 60 days. Clinical signs were central nervous impairment resulting in diminished control or loss of motor function and proprioception. Cytoplasmic vacuolar degeneration was a constant finding in the neurons of the central nervous system, and of the plexuses of Auerbach and Miessner. Cytoplasmic vacuoles were also present in reticuloendothelial cells, liver, kidney, and other parenchymatous organs. The contents of the vacuoles was not determined.

Dose response of sheep poisoned with locoweed (Oxytropis sericea)

Locoweed poisoning occurs when livestock consume swainsonine-containing Astragalus and Oxytropis species over several weeks. Although the clinical and histologic changes of poisoning have been described, the dose or duration of swainsonine ingestion that results in significant or irreversible damage is not known. The purpose of this research was to document the swainsonine doses that produce clinical intoxication and histologic lesions. Twenty-one mixed-breed wethers were dosed by gavage with ground Oxytropis sericea to obtain swainsonine doses of 0.0, 0.05, 0.1, 0.2, 0.4, 0.8, and 1.0 mg/kg/day for 30 days. Sheep receiving ≥0.2 mg/kg gained less weight than controls. After 16 days, animals receiving ≥0.4 mg/kg were depressed, reluctant to move, and did not eat their feed rations. All treatment groups had serum biochemical changes, including depressed α-mannosidase, increased aspartate aminotransferase and alkaline phosphatase, as well as sporadic changes in lactate dehydrogenase, sodium, chloride, magnesium, albumin, and osmolarity. Typical locoweed-induced cellular vacuolation was seen in the following tissues and swainsonine doses: exocrine pancreas at ≥0.05 mg/kg; proximal convoluted renal and thyroid follicular epithelium at ≥0.1 mg/kg; Purkinjes cells, Kupffers cells, splenic and lymph node macrophages, and transitional epithelium of the urinary bladder at ≥0.2 mg/kg; neurons of the basal ganglia, mesencephalon, and metencephalon at ≥0.4 mg/kg; and cerebellar neurons and glia at ≥0.8 mg/kg. Histologic lesions were generally found when tissue swainsonine concentrations were ≅150 ng/g. Both the clinical and histologic lesions, especially cerebellar lesions are suggestive of neurologic dysfunction even at low daily swainsonine doses of 0.2 mg/kg, suggesting that prolonged locoweed exposure, even at low doses, results in significant production losses as well as histologic and functional damage.

Polyhydroxy alkaloids: chromatographic analysis

Polyhydroxy alkaloids are a burgeoning category of natural products that encompass several structural types and generally exhibit potent activity as inhibitors of glycosidases. As presently defined the group consists of monocyclic or bicyclic aLkaloids of the pyrrolidine, piperidine, pyrrolizidine, indolizidine and tropane classes, bearing two or more hydroxyl groups. These structural features render the compounds highly water soluble and frequently quite insoluble in non-hydroxylic solvents, so that their isolation and analysis by chromatographic means are consequently difficult. This problem is further confounded by the lack of a chromophore which would permit their detection by UV absorption. This review presents chromatographic techniques that have been successfully applied to the problem of isolating, purifying, detecting and analyzing polyhydroxy alkaloids.

Toxicity of nitro-containing Astragalus to sheep and chicks.

Highlight: Several species of Astragalus that contain organic nitro compounds were tested for toxicity to sheep and l-week-old chicks. Methemoglobin analyses in sheep indicated that nitro compounds in A. diversifolius, A. convallarius, and A. pterocarpus resembled 3-nitro-1 -propanol in toxicity and rate of absorption from the digestive tract. Nitro compounds in A. cibarius and A. canadensis were more closely related to 3-nitropropanoic acid in toxicity and rate of absorption. A. pterocarpus, A. convallarius, and A. diversifolius have been categorized as “Class I” species because they produce acute oral toxicity in sheep at less than 100 mg NO2 fkg of body weight. “Class II” Astragalus (A. canadensis and A. cibariusj produce acute toxicity in sheep only if oral dosage exceeds 100 mg NO,/kg. Class I species are more likely to cause livestock losses on the range.