Ultrastructural observations in ponies after treatment with monensin.
Abstract: Ultrastructural studies were made of myocardium, diaphragm, appendicular muscle, liver, and kidney of 3 ponies acutely poisoned with a single oral dose of monensin (4 mg/kg of body weight). These ponies developed severe signs of toxicosis and were killed 28 to 72 hours after treatment. Severe mitochondrial damage (swelling) and lipoidosis in myocardial tissues were observed in 2 of the 3 ponies; similar, but less severe, changes were observed in the 3rd pony. The hepatocytes of the 3 ponies were characterized by increased amounts of smooth endoplasmic reticulum, large numbers of lipid droplets, vacuoles bounded by fibrous material, and a 2-fold increase in the number of peroxisomes per cell. Some hepatocytes also contained a membrane-bounded protein-like body. The observations indicate that heart mitochondria are primary targets of monensin poisoning in ponies.
Publication Date: 1981-01-01 PubMed ID: 7224315
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- Journal Article
Summary
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The research studied the effects of acute monensin poisoning in ponies. The study looked at the physical changes in a pony’s heart, diaphragm, muscle, liver, and kidney after administering monensin, and found that heart mitochondria are primarily affected.
Experimental Approach
- This study used ultrastructural studies, which are investigations at a microscopic level, to examine changes in the ponies’ hearts, diaphragms, muscles, livers and kidneys.
- The researchers administered a single oral dose of monensin to each of the three ponies in the experiment. The dose was equivalent to 4 mg/kg of the ponies’ body weight.
- The ponies were monitored and observed to develop severe signs of toxicosis, which is an extreme response to toxins. Given the severity of their symptoms, the ponies were euthanized between 28 to 72 hours after treatment for examination.
Research Findings
- The research primarily found substantial damage in the myocardium (heart muscle tissue) of two of the three ponies. Specifically, the mitochondria within these tissues were notably swollen, and lipoidosis (an overabundance of fat) was observed. This shows that the mitochondria of the heart muscle are particularly susceptible to monensin poisoning.
- The third pony also showed similar signs of mitochondrial swelling and lipoidosis, but these changes were less severe compared to the other two ponies.
- Microscopic examination of the liver cells (hepatocytes) of the three ponies also found physical changes, including an increase in the amount of smooth endoplasmic reticulum (a cellular structure involved in protein and lipid synthesis), a substantial increase in lipid droplets and vacuoles (small cavities in the cell often containing fluid), a twofold increase in the number of peroxisomes per cell (small cellular components involved in various metabolic processes), and the presence of a membrane-bound protein-like body within some hepatocytes.
Conclusion
- The findings of the study indicate that monensin poisoning in ponies primarily targets the mitochondria in the heart. The observed changes in other tissues like the liver also suggest the extensive systemic effects of this poison.
- The ultrastructural observations in this research provides valuable insights into the potentially fatal physiological responses to monensin toxicity in ponies, thus highlighting the need for careful usage and monitoring of such substances.
Cite This Article
APA
Mollenhauer HH, Rowe LD, Cysewski SJ, Witzel DA.
(1981).
Ultrastructural observations in ponies after treatment with monensin.
Am J Vet Res, 42(1), 35-40.
Publication
Researcher Affiliations
MeSH Terms
- Animals
- Female
- Furans / poisoning
- Horse Diseases / pathology
- Horses
- Liver / ultrastructure
- Male
- Microscopy, Electron
- Monensin / poisoning
- Myocardium / ultrastructure
Citations
This article has been cited 9 times.- Kastner N, Islam MN, Dybek M, Roth E, Heisinger S, Holy M, Jäntsch K, Walther D, Stockner T, Baumann MH, Brandt SD, Wallach J, Sitte HH, Kudlacek O. Prolintane analogs as hybrid monoamine transporter ligands: Structural determinants and species differences. J Biol Chem 2025 Dec;301(12):110903.
- Henn D, Lensink AV, Botha CJ. Ultrastructural changes in cardiac and skeletal myoblasts following in vitro exposure to monensin, salinomycin, and lasalocid. PLoS One 2024;19(9):e0311046.
- Votion DM. The story of equine atypical myopathy: a review from the beginning to a possible end. ISRN Vet Sci 2012;2012:281018.
- Cassart D, Fett T, Sarlet M, Baise E, Coignoul F, Desmecht D. Flow cytometric probing of mitochondrial function in equine peripheral blood mononuclear cells. BMC Vet Res 2007 Sep 28;3:25.
- Bourque JG, Smart M, Wobeser G. Monensis toxicity in lambs. Can Vet J 1986 Oct;27(10):397-9.
- Van Vleet JF, Ferrans VJ. Ultrastructural alterations in skeletal muscle of pigs with acute monensin myotoxicosis. Am J Pathol 1984 Mar;114(3):461-71.
- Van Vleet JF, Ferrans VJ. Ultrastructural alterations in the atrial myocardium of pigs with acute monensin toxicosis. Am J Pathol 1984 Mar;114(3):367-79.
- Van Vleet JF, Ferrans VJ. Myocardial diseases of animals. Am J Pathol 1986 Jul;124(1):98-178.
- Mollenhauer HH, Morré DJ, Rowe LD. Alteration of intracellular traffic by monensin; mechanism, specificity and relationship to toxicity. Biochim Biophys Acta 1990 May 7;1031(2):225-46.
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