ABSTRACT
The aging of skin has been associated with an increase in size of the adipocytes located within the subcutaneous tissue. This topic is the subject of our study conducted on rats clinically treated with L-acetyl-carnitine (LAC) at 4, 8, 16, and 21 months of age and on a control group. Normal rats showed a significant increase in adipocyte diameter between four and eight months, and between sixteen and twenty-one months of age. Rats treated with L-acetyl-carnitine did not show significant changes up to the age of sixteen months, but did so between sixteen and twenty-one months of age. Four-month-old rats, both those under treatment and controls, did not show a significant change in adipocyte diameter. On the other hand, rats receiving L-acetyl-carnitine showed significantly smaller adipocyte diameters than those of the control group. Our results demonstrate that the long-term administration of L-acetyl-carnitine blocks the progressive increase in size of the subcutaneous adipocytes present in the rat's aging skin. We hypothesize that L-acetyl-carnitine reequilibrates the catabolic deficit of fats in the skin of the elderly.
Subject(s)
Acetylcarnitine/pharmacology , Adipocytes/pathology , Cellular Senescence/drug effects , Connective Tissue/pathology , Skin/pathology , Adipocytes/drug effects , Animals , Cell Size/drug effects , Connective Tissue/drug effects , Evaluation Studies as Topic , Male , Rats , Rats, Wistar , Skin/drug effectsABSTRACT
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 resistant 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 and liver slices were obtained for transmission electron microscopy. As results obvious signs of primary and secondary microcholestasis associated to mitochondrial cristae detachment and phospholipid aggregations were noted; this last finding was less 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.
