Does stress influence ampicillin concentration in serum and tissues?

Exercise produces changes of drug levels in plasma and increases the concentration of free fatty acids (FFAs), which may interfere with drug-protein binding. FFAs seem to play an antagonistic role to drugs since they have a strong binding capacity to serum albumin. The aim of this study was to evaluate the influence of the consecutive exercise-induced stress in ampicillin levels. Two groups of Wistar rats were used. Group A consisted of six subgroups that were subjected to cold swimming (4 degrees C) for 5, 10, 15, 20,25, 30 days respectively. Group B was the control group. The animals were injected im. with ampicillin (1 g/Kg/8h in 5 doses). Results showed that exercise enhanced stress parameters (FFAs, adrenal weight, Ht%) and led to an ampicillin increase in all experimental groups comparatively to controls.

Changes in serum levels of quinolones in rats under the influence of experimental trauma.

Administration of antibiotics is considered an important factor during, or after, operational procedures in the maxillofacial area, in order to avoid post-surgical complications. In the present study, the levels of quinolones in serum and tissues such as the parotid gland, the tongue and the bone of the jaws were estimated during traumatic injury in the oral cavity. For this purpose, two groups (A and B) of Wistar rats, consisting of 35 animals each were used. Group A (control) and group B (experimental) were divided in five subgroups (A1, A2, A3, A4, A5, and B1, B2, B3, B4, B5). In the experimental group, model traumatic injury was performed through the whole lenght of the cheek. Subjects received orally ciprofloxacin, pefloxacin, norfloxacin, ofloxacin and cinoxacin. The concentration of quinolones in serum and in most of the tissues was significantly higher in the experimental groups than in controls. In addition, the FFA levels and the weight of adrenals (as indicators of stress) were higher in the trauma groups. Stress seemed to affect many pathophysiological mechanisms which are responsible for the alterations observed.

Expression of p53 and hsp70 in relation to apoptosis during Meckel's cartilage development in the mouse.

The process of Meckel's cartilage development was examined with regard to expression of p53, a tumor suppressor gene product and hsp70, a stress protein (heat-shock protein), in association with the occurrence of programmed cell death (apoptosis). Balb C mice embryos from embryonic days E13, E14, E15, E16, E17, E18 and 1- and 3-day-old pups were used. P53-positive cells were detected first at E15, and were found in the perichondrium of the distal part of Meckel's cartilage. During the degeneration process chondrocytes also became p53-positive. In contrast to p53, the expression of hsp70 was high and widespread in the early stages of development (E13-E15); however, it decreased with age, except for Meckel's cartilage, where hsp70 was found in the cytoplasm or nuclei of the hypertrophic cells. Apoptosis was first detected at E14-E15 in the perichondrium of the distal parts of Meckel's cartilage. The number of apoptotic bodies increased with age and the ongoing resorption of Meckel's cartilage. From the present study it can be concluded that expression of p53 and hsp70 varied during the development of Meckel's cartilage and that both proteins showed nuclear location in hypertrophic cells. No direct spatial or temporal correlation was observed between the expression of p53 and hsp70 and the occurrence of apoptotic bodies.