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Target Concepts:
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Query: UMLS:C0031117 (
peripheral neuropathy
)
10,577
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We examined 66 cats with salinomycin intoxication.
Salinomycin
caused different LMN signs of varying degrees of severity in all cases. Changes in blood work were unspecific, with the most frequent being increased serum creatine kinase activity, leukocytosis, and increased liver enzymes. Pathological electrodiagnostic findings: fibrillation potentials and positive sharp waves were detected in 10 cases, motor nerve conductance velocity was mildly decreased in 8/12 cats, and sensory nerve conductance velocity and repetitive nerve stimulation were normal in all examined cases. In five cases the
peripheral neuropathy
was confirmed by pathohistology. Fluid therapy and supportive care were used as therapy and 52 cats recovered completely. The probability for complete remission was significantly different between mildly and severely affected cases. It seems that the severity of clinical signs and prognosis correlate well with the amount of toxin ingested. We conclude that early recognition and decontamination combined with supportive care results in complete recovery.
...
PMID:Retrospective study of salinomycin toxicosis in 66 cats. 2044 77
Salinomycin
is a polyether antibiotic with properties of an ionophore, which is commonly used as cocciodiostatic drug and has been shown to be highly effective in the elimination of cancer stem cells (CSCs) both in vitro and in vivo. One important caveat for the potential clinical application of salinomycin is its marked neural and muscular toxicity. In the present study we show that salinomycin in concentrations effective against CSCs exerts profound toxicity towards both dorsal root ganglia as well as Schwann cells. This toxic effect is mediated by elevated cytosolic Na(+) concentrations, which in turn cause an increase of cytosolic Ca(2+) by means of Na(+)/Ca(2+) exchangers (NCXs) in the plasma membrane as well as the mitochondria. Elevated Ca(2+) then leads to calpain activation, which triggers caspase-dependent apoptosis involving caspases 12, 9 and 3. In addition, cytochrome c released from depolarized mitochondria directly activates caspase 9. Combined inhibition of calpain and the mitochondrial NCXs resulted in significantly decreased cytotoxicity and was comparable to caspase 3 inhibition. These findings improve our understanding of mechanisms involved in the pathogenesis of
peripheral neuropathy
and are important to devise strategies for the prevention of neurotoxic side effects induced by salinomycin.
...
PMID:Salinomycin induces calpain and cytochrome c-mediated neuronal cell death. 2163 91