Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The opsonizing capacity of sera from 22 patients with rheumatoid arthritis (RA), from 14 with psoriatic arthritis (AP), from seven with ankylosing spondylitis, and from healthy control persons was investigated by luminol-dependent chemiluminescence, induced during yeast phagocytosis of normal polymorphonuclear leukocytes. The chemiluminescence response using opsonizing sera was compared to that induced by no-opsonized yeast and the opsonizing capacity was expressed as a percentage. For the opsonization, fresh native serum, in some experiments Mg2+-EGTA and EDTA-treated serum, was used. In RA and AP sera, a significantly diminished opsonizing capacity (p less than 0.005) was observed. In healthy controls and in SPA patients, the opsonizing capacity of their sera was over 200%, while in seronegative RA patients, it was only 175%, in seropositive RA 125%, and in AP 150% was measured. There was no correlation between opsonizing capacity and complement or immunoglobulin content of the investigated sera. The amount of C3b, IgG and IgM covalently bound to yeast particles was determined, too. Yeast particles bind significantly less (p less than 0.01) IgG when opsonized with RA and AP sera, while a higher relative amount of IgM (p less than 0.01) was bound to yeast incubated in the sera of seropositive RA patients. No significant differences in the C3b binding were observed.
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PMID:[Defects in opsonization activity of the serum of patients with chronic arthritis]. 321 63

Diclofenac (DCLF) is a nonsteroidal anti-inflammatory drug that is widely used for the treatment of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and acute muscle pain conditions. Toxic doses of DCLF can cause nephrotoxicity in humans and experimental animals. However, whether this DCLF-induced nephrotoxicity involves apoptotic cell death in addition to necrosis is unknown. The goals of this investigation were to determine whether DCLF-induced nephrotoxicity involves oxidative stress and apoptotic type genomic DNA fragmentation, and if so, whether DCLF-induced oxidative stress and DNA fragmentation cause apoptotic cell death in mouse kidneys. Male ICR mice (CD-1; 25-45 g), fed ad libitum, were administered nephrotoxic doses of DCLF (100, 200, 300 mg/Kg, po) and sacrificed 24 h later. Blood was collected to evaluate renal injury (BUN), lipid peroxidation (MDA: malondialdehyde levels), and superoxide dismutase (SOD) activity (a marker of oxidative stress). Kidney tissues were analyzed both quantitatively and qualitatively to determine the degree and type of DNA damage, and evaluated histopathologically for the presence of apoptotic characteristics in the nucleus of diverse types of kidney cells. Results show that diclofenac is a powerful nephrotoxicant (at 100, 200, and 300 mg/kg: 4.7-, 4.9-, and 5.0-fold increases in BUN compared to the control, respectively) and a strong inducer of oxidative stress (significant increase in MDA levels). Oxidative stress induced by DCLF was also coupled with massive kidney DNA fragmentation (100, 200, and 300 mg/kg: 3-, 8-, and 10-fold increases compared to control, respectively). A dose-dependent increase in MDA levels and SOD activity was also observed, which indicated a link between oxidative stress and nephrotoxicity. Qualitative analysis of DNA fragmentation by gel electrophoresis showed a DNA ladder indicative of Ca2+-Mg2+-endonuclease activation. Histopathological examination of kidney sections revealed numerous apoptotic nuclei across proximal and distal tubular cell linings. Collectively, these data for the first time suggest that DCLF-induced nephrotoxicity may involve production of reactive oxygen species leading to oxidative stress and massive genomic DNA fragmentation, and these two free radical mediated events may ultimately translate into apoptotic cell death of kidney cells in vivo, and reveal a DNA-active role for DCLF.
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PMID:Diclofenac induced in vivo nephrotoxicity may involve oxidative stress-mediated massive genomic DNA fragmentation and apoptotic cell death. 1144 Aug 26