Amikacin-induced liver toxicity: correlations between biochemical indexes and ultrastructural features in an experimental model
G. Martines
(Inicie sesión)
,
L. Butturini
(Inicie sesión)
,
I. Menozzi
(Inicie sesión)
,
G. Restori
(Inicie sesión)
,
L. Boiardi
(Inicie sesión)
,
S. Bemardi
(Inicie sesión)
,
P. Baldassarri
(Inicie sesión)
Barra lateral del artículo
174)
Publicado:
mar 23, 2017
Cómo citar
Martines, G., Butturini, L., Menozzi, I., Restori, G., Boiardi, L., Bemardi, S., & Baldassarri, P. (2017). Amikacin-induced liver toxicity: correlations between biochemical indexes and ultrastructural features in an experimental model. Revista De Medicina De La Universidad De Navarra, 32(1), 41-45. https://doi.org/10.15581/021.7218
Contenido principal del artículo
Autores/as
G. Martines
(Inicie sesión)
L. Butturini
(Inicie sesión)
I. Menozzi
(Inicie sesión)
G. Restori
(Inicie sesión)
L. Boiardi
(Inicie sesión)
S. Bemardi
(Inicie sesión)
P. Baldassarri
(Inicie sesión)
Resumen
55
In previous studies, aminoglycosides (AG) as gentamicin (G), dibekacin (D), tobramycin (T), netilmicin (N) and Sysomicin (S) were proved to induce ultrastructural alterations in the liver of experimental animals.
The aim of this studies is to investigate the effect of amikacin (AK) on rabbit liver which is commonly used in infections resistent to other AG; this was done studying both the common blood parameters and ultrastructural changes.
The study was accomplished in 24 New-Zealand rabbits, twelve received 20 mg/kg AK every 12 hours for 2 weeks.
Thereafter the animals were anesthesized ane liver slices were obtained for transmission electron microscopy.
As results obvious signs of primary and secondary microcholestasis associated to mitochondral cristae detachment and phospholipid aggregations were noted; this last finding was Jess marked when compared to previous studies employing other AG.
In the AK treated group, blood tests showed a significant increased in only Blood Urea Nitrogen (BUN) and an insignificant rise in AST levels.
Our findings are consistent with an AK induced liver toxicity albeit less evident with respect to the other AG.
The aim of this studies is to investigate the effect of amikacin (AK) on rabbit liver which is commonly used in infections resistent to other AG; this was done studying both the common blood parameters and ultrastructural changes.
The study was accomplished in 24 New-Zealand rabbits, twelve received 20 mg/kg AK every 12 hours for 2 weeks.
Thereafter the animals were anesthesized ane liver slices were obtained for transmission electron microscopy.
As results obvious signs of primary and secondary microcholestasis associated to mitochondral cristae detachment and phospholipid aggregations were noted; this last finding was Jess marked when compared to previous studies employing other AG.
In the AK treated group, blood tests showed a significant increased in only Blood Urea Nitrogen (BUN) and an insignificant rise in AST levels.
Our findings are consistent with an AK induced liver toxicity albeit less evident with respect to the other AG.
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