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Home » [Update] Cycadophyta – an overview | cycadophyta – NATAVIGUIDES

[Update] Cycadophyta – an overview | cycadophyta – NATAVIGUIDES

cycadophyta: คุณกำลังดูกระทู้

Konnie H. Plumlee DVM, MS, Dipl ABVT, ACVIM , … Patricia A. Talcott , in Clinical Veterinary Toxicology, 2004

Synonyms.

Cycad palms are known as sago palms (Cycas cirinalis), Japanese cycad (Cycas revoluta), cardboard palms (Zamia furfuracea), coontie plants (Zamia pumila), or simply by their genus Cycads, Zamias, or Macrozamia.1-4

Sources.

The members of the Cycadales order include three families: Cycadaceae (with one genus, Cycas), Stangeriaceae (with a single species, Stangeria eriapus), and Zamiaceae (with eight genera, of which Zamia species are encountered most frequently in the United States).3-6 These plants are palmlike in appearance and are native to tropical and subtropical climates around the world. They have been used for many years as a food source and for medicinal purposes.7 Lately, their increased use as ornamental houseplants has made them available all over the world.6,8 The Cycadales order includes both male and female plants in each species, and only the female plant produces the nuts (seeds).1,2,4

Toxicokinetics.

Cycad palms have three types of toxins.1,2,4,8

1.

Cycasin is the major glycoside present in Cycads. Cycasin is converted to its aglycone methylazoxymethanol (MAM) by β-glucosidases. These β-glucosidases can be found in the skin of newborn animals or in the gastrointestinal tract of most other animals.

2.

β-methylamino-L-alanine (BMAA) is a neurotoxic amino acid.

3.

An unidentified toxin with a high molecular weight.

No specific information is known about the kinetics of the cycad toxins in humans or animals. However, signs of toxicosis in dogs usually occur within 12 to 24 hours of ingestion.3,8,9 In cattle, the hindlimb paralysis may take several days to appear. These neurologic signs also require long-term ingestion of the cycad plants.1,8 In sheep fed Macrozamia redlei nuts, chronic liver disease developed over a period of 3 to 11 months.1

Mechanism of Action.

Cycasin irritates the gastrointestinal tract and causes hepatic necrosis.1,8 This glycoside is also carcinogenic, mutagenic, and teratogenic.1,2,4,8 The toxic amino acid BMAA causes ataxia in rats, but is not the cause of hindlimb ataxia in cattle.4 Rats given high doses of BMAA developed necrosis of the neurons in the cerebellum, causing the rats to become ataxic.1,10 Although the mechanism is not known, BMAA has also been implicated as the cause of Guam disease in humans. The third major toxin in cycad palms is unknown at this time. This toxin is suspected of causing axonal degeneration in the central nervous system (CNS).2,4,8

Toxicity and Risk Factors.

Because of the multiple toxins inherent in cycads and the varying habits of each animal species, different syndromes are caused by cycad ingestion. Cattle prefer to eat leaves, but sheep and dogs are known to consume leaves and seeds.7-9 In fact, dogs have consumed all parts of the cycad plant, including the roots.9 Sheep frequently ingest seeds and leaves and often ingest large amounts at a time.

Cycasin is thought to be responsible for the hepatic and gastrointestinal signs seen in sheep and dogs after the plants are eaten.1,4 Nuts (seeds) contain a higher amount of the glycosides (cycasin) than do other parts of the plant. Dogs that develop signs most often ingest seeds or have been chewing on the plants and roots.9 As few as two seeds ingested by dogs can cause signs.11

BMAA has caused ataxia in rats but is unlikely to be involved in the cause of zamia staggers in cattle.10 The doses of BMAA used in rats to cause ataxia were a very large amount compared to what an animal might be exposed to when eating the whole cycad plant. Its effect in causing disease in most animals is unknown.1,10

The unidentified toxin in cycads is thought to be the cause of hindlimb paralysis in cattle resulting from axonal degeneration in the central nervous system.1,4 Cattle usually must consume the plants for extended periods of time before any signs appear.7-9

Clinical Signs.

Most animals are affected by either the gastrointestinal and hepatic disease syndrome or the ataxia and central nervous disease syndrome. These differences in disease are probably a result of the different doses consumed by the animals, their duration of exposure, and the parts of the cycad plant ingested.1,7,9

In dogs, the most commonly reported clinical sign following cycad ingestion is vomiting (with or without blood).9 Depression, diarrhea, and anorexia have also been reported frequently. Seizures did occur in some cases, but the seizures were usually thought to be secondary to hepatic damage. Even though deaths have been reported, most dogs survived with appropriate supportive care.9

The customary signs reported after sheep have ingested cycads are lethargy, anorexia, weight loss, and gastroenteritis (which may or may not be hemorrhagic).1,7 Both dogs and sheep consume more of the cycad glycosides.7-9 Massive outbreaks of disease in sheep have been reported and death occurs frequently.1

In cattle, frequently reported signs include weight loss, weakness, ataxia, and paresis (a syndrome called zamia staggers). However, the cattle have often been exposed for several days, which made determining the etiology of the disease difficult.1,7 Although cattle are more frequently affected by CNS disease, it is still possible to see hepatic damage in cattle after cycad ingestion.1,7

Clinical Pathology.

Elevated serum ALT, AST, and alkaline phosphatase are commonly reported in dogs ingesting cycads. Hyperbilirubinemia and electrolyte abnormalities are also often noted. Increased BUN and leukocytosis have occasionally been reported in dogs.9

Clinically affected ruminants may develop leukocytosis, hypoalbuminemia, and elevations of AST, alkaline phosphatase, and GGT. Hypocholesterolemia and decreased triglyceride levels were also noted in several heifers after the consumption of cycad plants for an undetermined amount of time.7

Lesions.

Gastrointestinal lesions in dogs with cycad poisoning include hemorrhage and necrosis of gastrointestinal mucosa.8 Focal necrosis and ulceration of the abomasum have been reported in sheep.1 Dairy heifers exposed to cycad plants did not develop any gastrointestinal lesions.7

Histologic lesions in the liver of dogs ingesting cycad plants include cirrhosis, marked focal centrolobular, and midzonal coagulation necrosis.8 The principal hepatic lesions in ruminants ingesting cycad plants are megalocytosis, periacinar necrosis, and fibrosis.1

Some animals with hepatic disease caused by cycad ingestion may develop hepatic encephalopathy. Characteristic nervous signs and spongy degeneration of the central nervous system may be present.1 Other brain and spinal cord lesions include demyelination and axonal degeneration in brain, spinal cord, and dorsal root ganglia.7

Diagnostic Testing.

Often identifiable fragments of the cycad plant or seeds are found in the stomach or intestinal contents of poisoned animals. Although cycasin and BMAA can be found in the liver of animals that ingest cycad palms, no diagnostic laboratories routinely test for these compounds.

Treatment.

Emesis and activated charcoal help prevent signs in animals that have recently ingested cycads. However, if it has been longer than 2 to 4 hours since the plant material was ingested, emesis is not likely to have any benefit because the stomach is probably empty by then.9 In addition, inducing emesis in a symptomatic animal is often contraindicated. If the ingestion occurred less than 12 hours earlier, activated charcoal prevents further absorption of the cycad toxins.9,11 In some cases, multiple doses of activated charcoal may be beneficial.

No antidote for any of the cycad toxins is available. Consequently, treatment of poisoned animals focuses on supportive and symptomatic care. Companion animals can be given gastrointestinal protectants such as sucralfate (1 g in large dogs, 0.5 g in small dogs orally every 8 hours), H2 blockers such as cimetidine (5 to 10 mg/kg intravenously or by mouth every 8 hours), or misoprostol (1 to 3 μg/kg).12 Fluid and electrolyte support is beneficial and should be used as needed. The fluid of choice for animals with hepatic damage is 5% dextrose.13 Blood transfusions may be necessary if gastrointestinal tract hemorrhage is severe.9,13,14

Prognosis.

The prognosis is good if the animal is decontaminated before the onset of clinical signs. Prognosis is guarded when animals are showing signs. Surviving cattle with neurologic signs have remained ataxic and have had secondary atrophy of hindlimb musculature for the remainder of their lives.7 The disease could lead to lifelong hepatic support in animals with hepatic damage.7,8,9

Prevention and Control.

The young leaves of cycad plants are considered to be very palatable. Cattle and sheep preferentially seek out the cycad palms.3,7,8,11 All animals should be denied access to areas that contain cycad palms, or the palms should be destroyed.

[Update] Cycadophyta – an overview | cycadophyta – NATAVIGUIDES

1.23.3.1.4(i) Gymnosperms

Cycads are often considered to be the most basal extant group of seed plants, with a fossil record dating back to the late Carboniferous (∼300   Ma, Figure 4); nevertheless, the true evolutionary relationship between gymnosperm groups is at present still not certain.52–54 There are ∼300 species of cycads, distributed mainly through tropical and subtropical areas,55 but their phytochemistry is not well explored. Nevertheless, the presence of both allyl- and propenylphenol derivatives in the volatiles from male and female cones of one cycad, Cycas revoluta,56 appears to be on a firmer footing relative to the algae and horsetail reports above. Based on GC–MS analysis, together with comparison of the corresponding authentic standards, methylchavicol (3) was established as the primary component (∼67–93%) of its volatiles, together with smaller amounts of anethole (5) and methyleugenol (42). To date, however, this is the only cycad known reportedly producing this class of natural products.

Conifers (Pinophyta) are thought to have emerged as early as the late Carboniferous (∼310   Ma),57,58 and now comprise ∼630 extant species.59 An initial review of the literature8 suggested the absence of allyl-/propenylphenols proper in pine and hemlock (as well as poplar), except for numerous accounts of eugenol (4)/isoeugenol (6) being detected following pyrolysis GC–MS of presumed lignin-containing conifer tissues, for example, see Faix et al.60 and Camarero et al.61 Such moieties are considered generated by the pyrolysis of monolignol-derived metabolites, including polymeric lignins.

A recent, more in-depth, analysis using the specific structures for searching rather than compound names gave a somewhat different perspective. This resulted in the identification of a relatively small number of papers reporting complex mixtures of various essential oils and oleoresins obtained from either needles, bark, wood, or wounded stem tissue of nine pine (Pinus),62–72 one spruce (Picea),65 one Tasmanian conifer (Lagarostrobos franklinii),73 and three juniper (Juniperus)74 species. Buried within the tables in these studies, in addition to the plethora of mono-, sesqui-, and diterpenes, various allyl-/propenylphenols were detected in low to trace amounts, for example, methylchavicol (3) in seven of nine pine species examined,62–64,66–70,72 with Pinus taeda69 and Pinus ponderosa72 also having methyleugenol (42). Three of these pines (P. brutia,71 P. contorta,62 and P. sylvestris65) as well as spruce (Picea abies)65 reportedly also contained anethole (5), with methyleugenol (42) and (E)-methylisoeugenol (43) being detected in P. brutia71 as well. In addition, the oil of L. franklinii wood was shown to contain 42, 43, and elemicin (45).73 Anethole (5) was also detected in J. brevifolia, and (E)-methylisoeugenol (43) in Juniperus formosana and Juniperus rigida, whereas seven other juniper species apparently contained no allyl-/propenylphenols.74 These data would thus suggest that both allyl- and propenylphenols can be present in these organisms. However, when the essential oil yields were taken into account, the overall amounts of these allyl-/propenylphenols were very low, that is, ranging from 0.002 to 0.06% of dry weight.

The detection of these substances, at trace to very low levels in the essential oil fractions, raises some interesting questions as to whether they are true gymnospermous natural products or, albeit less likely, result from other effects of an encroaching predator/pathogen, for example, through insect or pathogen attack with conversion of plant-derived monolignol-/lignin-derived components, resulting in release of trace amounts of such substances. Such reports emphasize the need, however, for a full biochemical clarification to better understand the true chemotaxonomical significance of such observations.

Currently, there are no reports of allyl-/propenylphenols in either the Gnetales (which are thought to have emerged ∼270   Ma)75 or in Ginkgo biloba (the single remaining extant species of the Ginkgoaceae family, which is considered to have emerged at least ∼170   Ma, see Figure 4).76 Taken together, the evolutionary significance of this apparently scattered chemotaxonomy in the gymnosperms is, at present, not well understood.


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How To Say Cycadophyta

BIOTODOMA cupido, CUPID CICHLIDS in Nature – Rio ARAGUAIA PART 1


Cupid cichlids (Biotodoma cupido) are widespread in the Amazon basin, but never common in the river. Check out this beautiful cichlid defending their nest in the flood zone of the upper Araguaia River in Brazil.
Check in for Part 2 with a new Crenicichla, wolf fish and Heros next week!
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CORYDORAS https://youtu.be/MMsj6H5E4qo
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BIOTODOMA cupido, CUPID CICHLIDS in Nature - Rio ARAGUAIA PART 1

Life cycle of Phylum Cycadophyta ( Cycas ) AL Biology Sinhala


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Life cycle of Phylum Cycadophyta ( Cycas )  AL Biology Sinhala

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Phylum Cycadophyta


Phylum Cycadophyta

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