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Results for “Paromomycin”

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At least 217 records · Page 12Linked to original sources
PubMed1997

Comparison of aminosidine (paromomycin) and sodium stibogluconate for treatment of canine leishmaniasis.

Twelve dogs naturally infected with Leishmania infantum were treated subcutaneously with aminosidine at a dose of 10 mg kg-1 per day for four weeks. Antimonial compounds were used as reference drugs in twelve Leishmania-infected dogs. Eleven of the twelve dogs submitted to aminosidine therapy responded within 30 days. The treatment with the aminoglycoside antibiotic presented a marked decrease of anti-Leishmania antibody titres than the controls. Aminosidine also reduced urinary protein, serum IgG, and circulating immune complex concentrations. Side effects were observed only in a dog with pre-existent renal lesions. This study proved that aminosidine is an effective, tolerable and safe drug for the treatment of canine leishmaniasis and that it could be used as a suitable substitute for antimonial therapy.

Amebicides↗
PubMed2005

Mutations in MTO2 related to tRNA modification impair mitochondrial gene expression and protein synthesis in the presence of a paromomycin resistance mutation in mitochondrial 15 S rRNA.

Nuclear gene(s) have been shown to modulate the phenotypic expression of mitochondrial DNA mutations. We report here the identification and characterization of the yeast nuclear gene MTO2 encoding an evolutionarily conserved protein involved in mitochondrial tRNA modification. Interestingly, mto2 null mutants expressed a respiratory-deficient phenotype when coexisting with the C1409G mutation of mitochondrial 15 S rRNA at the very conservative site for human deafness-associated 12 S rRNA A1491G and C1409T mutations. Furthermore, the overall rate of mitochondrial translation was markedly reduced in a yeast mto2 strain in the wild type mitochondrial background, whereas mitochondrial protein synthesis was almost abolished in a yeast mto2 strain carrying the C1409G allele. The other interesting feature of mto2 mutants is the defective expression of mitochondrial genes, especially CYTB and COX1, but only when coexisting with the C1409G allele. These data strongly indicate that a product of MTO2 functionally interacts with the decoding region of 15 S rRNA, particularly at the site of the C1409G or A1491G mutation. In addition, we showed that yeast and human Mto2p localize in mitochondria. The isolated human MTO2 cDNA can partially restore the respiratory-deficient phenotype of yeast mto2 cells carrying the C1409G mutation. These functional conservations imply that human MTO2 may act as a modifier gene, modulating the phenotypic expression of the deafness-associated A1491G or C1409T mutation in mitochondrial 12 S rRNA.

Alleles↗