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Fatty acids resources:

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Clin Nephrol. 2002 Jul;58 Suppl 1:S20-5.
Elevated serum concentration of cardiotoxic lipid peroxidation products in chronic renal failure in relation to severity of renal anemia.

Siems W, Carluccio F, Grune T, Jakstadt M, Quast S, Hampl H, Sommerburg O.

Herzog Julius Hospital, Bad Harzburg, Germany. Werner.Siem-online.de

Patients with end-stage renal disease undergoing hemodialysis (HD) are exposed to oxidative stress. Increased levels of malondialdehyde (MDA) and 4-hydroxylnonenal (HNE) were found in plasma of uremic patients indicating accelerated lipid peroxidation (LPO) as a consequence of multiple pathogenetic factors. The catabolism and action of those products was already intensively studied. As highly reactive metabolites they are able to bind to proteins, nucleic acids, and other molecules. Doing so, they exert molecular signal effects in cells and are able to exacerbate tissue and organ damage, e.g. cardiotoxic effects. Since renal anemia was shown to promote oxidative stress as well, the aim of our investigation was to examine its role in HD patients. Therefore, two groups of HD patients were investigated (group I Hb < 10 g/dl, group II Hb > 10 g/dl) and serum concentrations of MDA, HNE, and of protein carbonyls, a marker for protein oxidation, were determined. All HD patients had significantly higher levels of the LPO products MDA and HNE compared with controls. However, group I patients showed higher MDA and HNE concentrations compared to group II patients. The same result could be seen for protein carbonyls. During HD concentration of both LPO products decreased. However, this was not the case for protein carbonyls. These results lead to the conclusion that optimized correction of the renal anemia may result in a significant reduction of oxidative stress and therefore in the reduction of organ tissue damage. In this way correction of renal anemia will reduce the cardiovascular risk and comorbidity of HD patients improving their prognosis.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12227722&dopt=Abstract



Clin Nephrol. 2002 Jul;58 Suppl 1:S31-6.
Adaptation of glutathion-peroxidase activity to oxidative stress occurs in children but not in adult patients with end-stage renal failure undergoing hemodialysis.

Sommerburg O, Grune T, Ehrich JH, Siems WG.

Department of Pediatrics, University Hospital Ulm, Germany. olaf.sommerbur-online.de

Lipid peroxidation (LPO) products formed after reaction of free radicals with membrane lipids are involved in the pathogenesis of cardiac diseases. Also in patients with end-stage renal disease (ESRD) LPO was shown to be accelerated and concentrations of non-enzymatic antioxidants were measured lower than in control subjects. However, up to now only limited knowledge about the role of antioxidant enzymes was available. Whether or not activity of those antioxidants might be induced due to oxidative stress in ESRD patients is not known. To answer the question the activity of 3 enzymatic antioxidants, superoxide dismutase (SOD), catalase (CAT), and glutathion peroxidase (GPx), was measured in red blood cells of the ESRD patients undergoing hemodialysis (2 groups: children and adults) and matching controls. LPO in these subjects was determined by measurement of the LPO product 4-hydroxynonenal (HNE) in blood plasma. Plasma HNE was significantly increased by factor 3 in both patient groups children and adults compared to the control groups. The activity of the enzymatic antioxidants was measured differently. While SOD was significantly lower in patients (children and adults) than in the matching controls this was not the case for catalase and GPx. While GPx activity in adult patients was comparable to that in the control groups (childrens and adults), the GPx in children with ESRD was almost twice as high than in the other groups. Since children were shown to have higher levels of glutathion, activated GPx might be a sign of adaptation of these children to the increased rate of oxidation.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12227724&dopt=Abstract



J Toxicol Environ Health A. 2002 Sep 27;65(18):1333-50.
Altered gene expression profiles of rat lung in response to an emission particulate and its metal constituents.

Nadadur SS, Kodavanti UP.

Pulmonary Toxicology Branch, ETD, NHEERL, ORD, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA. nadadur.srikantpa.gov

Comprehensive and systematic approaches are needed to understand the molecular basis for the health effects of particulate matter (PM) reported in epidemiological studies. Due to the complex nature of the pollutant and the altered physiological conditions of predisposed populations, it has been difficult to establish a direct cause and effect relationship. A high-throughput technology such as gene expression profiling may be useful in identifying molecular networks implicated in the health effects of PM and its causative constituents. Differential gene expression profiles derived for rat lungs exposed to PM and its constituent metals using a custom rat cardiopulmonary cDNA array are presented here. This array consists of 84 cardiopulmonary-related genes representing various biological functions such as lung injury/inflammation, repair/remodeling, structural and matrix alterations, and vascular contractility, as well as six expressed sequence tags (ESTs). The cDNA array was hybridized with (32)P-labeled cDNA generated from rat lung RNA. Total lung RNA was isolated from male Sprague-Dawley rats at 3 and 24 h following intratracheal instillation of either saline, residual oil fly ash (ROFA; 3.3 mg/kg), or its most toxic metallic constituents, nickel (NiSO(4); 3.3 mmol/kg) and vanadium (VSO(4); 5.7 mmol/kg). Metal concentrations reflected the levels present in one ROFA instillate. Densitometric scans of the array blots indicated ROFA- and metal-specific increased expression (1.5 to 3-fold) of stress response, inflammatory, and repair-related genes, and also genes involved in vascular contractility and thrombogenic activity. Expression of multiple cytokines in ROFA exposed rat lung compared to Ni and V suggest the role and importance of understanding constituent interactions in PM toxicity. Expression profiling using genomic approaches will aid in our understanding of toxicant-specific altered molecular pathways in lung injury and pathogenesis.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12227955&dopt=Abstract



emory.edu

Neisseria meningitidis (meningococcus), an exclusive pathogen of humans, is the cause of sepsis (meningococcemia) and meningitis, often in otherwise healthy individuals. Several hundred thousand cases of meningococcal disease occur worldwide each year, a number that is frequently accentuated by epidemic outbreaks. In recent years, significant advances, fueled by new molecular approaches and genome sequencing projects, have improved our understanding of the pathogenesis of meningococcal disease and have led to progress in the development of the next generation of meningococcal vaccines. However, the mortality of meningococcal disease remains 10% to 15% for all cases, and is up to 40% in patients with severe sepsis. This review summarizes current knowledge of the pathogenesis, therapy, and prevention of meningococcal disease with emphasis on meningococcal sepsis.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12228024&dopt=Abstract [PubMed - as supplied by publisher]



Curr Infect Dis Rep. 2002 Oct;4(5):387-399.
The Pathophysiology and Treatment of Candida Sepsis.

Spellberg B, Edwards JE.

Division of Infectious Diseases, Harbor-UCLA Medical Center, St. Johns Cardiovascular Research Center, Research and Education Institute, 1124 West Carson Street, Torrance, CA 90502, USA. bjumc.edu; edwardumc.edu

Sepsis can occur during disseminated candidiasis, but its pathogenesis differs from that caused by typical prokaryotic pathogens. Complex interactions between defects in host defense and "relative" virulence factors expressed by Candida lead to dissemination of the saprophyte to parenchymal organs, and subsequently to onset of multiorgan failure. This review focuses first on the pathophysiology of Candida sepsis, detailing current understanding of host-pathogen interactions. We then consider the choice of antifungal and supportive treatments.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12228025&dopt=Abstract [PubMed - as supplied by publisher]







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