Stamatia Levidiotou | PubMed Health

PubMed2003

Acute-phase response to benzo[a]pyrene and induction of rat ALDH3A1.

The aldehyde dehydrogenase-3A1 (ALDH3A1) enzyme, encoded by a member of the [Ah]-gene family, is dramatically increased (more than 100-fold) by benzo[a]pyrene (BaP) and other polycyclic hydrocarbons. Although much is known regarding the mechanism for the drug-metabolizing enzymes up-regulated by the Ah receptor, the physiological role of that tremendously increased ALDH3A1 enzyme activity is not yet fully clarified. The aim of this study was to identify a possible acute-phase response to different classes of xenobiotics affecting the metabolic capacity of the hepatocyte, by studying possible changes of serum acute-phase proteins (APPs) of hepatic origin, before and after BaP administration. Male Wistar rats were used in different series of experiments. The effects of BaP were estimated in terms of dose-response and time-response, with regard to the serum level of several APPs such as alpha-1-acid-glycoprotein (AAG), alpha-1-antitrypsin (AAT), C-reactive protein (CRP), and haptoglobin (HPT). In parallel experiments, levels of the same proteins have been determined after a time-dependent treatment with lipopolysaccharide (LPS). The changes in serum proteins were compared with the results of BaP or LPS administration on both hepatic ALDH3A1 and total ALDH enzyme activities. The results showed that BaP induced CRP and HPT in a time-dependent way, proportional to that caused by LPS. Additionally, ALDH3A1, CRP, and HPT were induced by BaP subacute treatment, whereas another type of ALDH inducer, phenobarbital, did not affect the levels of APPs or ALDH3A1, but did increase ALDH1A3 activity. Former studies of our group have shown that the inhibitory effects of different non-steroidal anti-inflammatory drugs (NSAIDs) on the ALDH3A1 induction were most possibly due to a decreased formation of arachidonic products like prostaglandins. Considering the changes of APPs caused by BaP, this study further supports the suggestion that the induction of ALDH3A1 is related to an atypical hepatocyte inflammation produced by xenobiotics.

Acute-Phase Proteins↗

PubMed2002

Neonatal bacteraemia: a population-based study.

The aims of this study were to explore the incidence of neonatal bacteraemia and identify the risk factors among neonatal intensive care unit (NICU) patients. The study included 3339 neonates admitted to the NICU of Ioannina University Hospital, North-Western Greece, during the 10-y period 1989-98. Logistic regression was used to assess the contribution of different risk factors to bacteraemia. A diagnosis of bacteraemia was made in 90 neonates (2.7%), 10 of whom (11%) died. Gram-negative bacilli, coagulase-negative Staphylococci and Streptococci were the most common pathogens: 42%, 34% and 17%, respectively. Premature rupture of membranes was the main risk factor for early-onset sepsis (relative risk 6.28) and respiratory distress syndrome was the main risk factor for late-onset sepsis (relative risk 5.70). The relative size of neonates for their gestational age did not appear to influence the risk of infection. Case fatality was higher for early- than for late-onset sepsis (relative risk 6.59). In conclusion, certain conditions were confirmed to predispose patients to neonatal bacteraemia; neonatal morbidity and mortality can be reduced by intervening to control these predisposing factors.

Bacteremia↗