Advanced glycation and lipidoxidation of the peritoneal membrane: Respective roles of serum and peritoneal fluid reactive carbonyl compounds

Miyata, Toshio; Horie, Kuniaki; Ueda, Yoshimichi; Fujita, Yuji; Izuhara, Yuko; Honda, Hiroshi; Uchida, Kôji; Saitō, Akira; Strihou, Charles van Ypersele de; Kurokawa, Kiyoshi

doi:10.1046/j.1523-1755.2000.00182.x

Cited by 123 publications

(109 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In this study, we demonstrate that neither olmesartan, an AIIR antagonist, nor temocaprilat, an ACE inhibitor, entrap and lower in vitro the concentration of two RCO, glyoxal and methylglyoxal. This finding stands in contrast with aminoguanidine and OPB-9195, both of which, at equimolar concentrations, markedly reduce the levels of both RCO, confirming previous observations (28). Pyridoxamine has an intermediary effect.…”

Section: Discussionsupporting

confidence: 90%

See 1 more Smart Citation

Angiotensin II Receptor Antagonists and Angiotensin-Converting Enzyme Inhibitors Lower In Vitro the Formation of Advanced Glycation End Products

Miyata¹,

Strihou²,

Ueda³

et al. 2002

Journal of the American Society of Nephrology

Self Cite

282

218

View full text Add to dashboard Cite

Abstract. The implication of advanced glycation end products (AGE) in the pathogenesis of atherosclerosis and of diabetic and uremic complications has stimulated a search for AGE inhibitors. This study evaluates the AGE inhibitory potential of several well-tolerated hypotensive drugs. Olmesartan, an angiotensin II type 1 receptor (AIIR) antagonist, as well as temocaprilat, an angiotensin-converting enzyme (ACE) inhibitor, unlike nifedipine, a calcium blocker, inhibit in vitro the formation of two AGE, pentosidine and N ⑀ -carboxymethyllysine (CML), during incubation of nonuremic diabetic, nondiabetic uremic, or diabetic uremic plasma or of BSA fortified with arabinose. This effect is shared by all tested AIIR antagonists and ACE inhibitors. On an equimolar basis, they are more efficient than aminoguanidine or pyridoxamine. Unlike the latter two compounds, they do not trap reactive carbonyl precursors for AGE, but impact on the production of reactive carbonyl precursors for AGE by chelating transition metals and inhibiting various oxidative steps, including carbon-centered and hydroxyl radicals, at both the pre-and post-Amadori steps. Their effect is paralleled by a lowered production of reactive carbonyl precursors. Finally, they do not bind pyridoxal, unlike aminoguanidine. Altogether, this study demonstrates for the first time that widely used hypotensive agents, AIIR antagonists and ACE inhibitors, significantly attenuate AGE production. This study provides a new framework for the assessment of families of AGE-lowering compounds according to their mechanisms of action.Advanced glycation and oxidation irreversibly modify proteins over the years and thus contribute to aging phenomena (1). Their local or generalized acceleration is associated with atherosclerosis (2-6) as well as with various diabetic (7-10) and uremic complications (11-13). Inhibition of advanced glycation end products (AGE) formation has thus become a therapeutic goal.Aminoguanidine, the first AGE inhibitor discovered in 1986 (14), and (Ϯ)-2-isopropylidenehydrazono-4-oxo-thiazolidin-5-ylacetanilide (OPB-9195) (15) are both hydrazine-derivatives. They inhibit in vitro the formation of AGE, pentosidine (16), and N ⑀ -carboxymethyllysine (CML) (17) from a variety of individual precursors, such as ribose, glucose, and ascorbate, as well as that of advanced lipoxidation end products (ALE), malondialdehyde-lysine and 4-hydroxynonenal-protein adduct (18), from arachidonate (19). They also inhibit pentosidine generation in diabetic and uremic plasma incubated for 4 wk (20).As expected, both compounds correct several biologic effects that are associated with AGE formation. In murine thymocyte and fibroblasts, they inhibit the phosphorylation of tyrosine residues of a number of intracellular proteins induced by cell surface Schiff base formation (21). Given to diabetic animal models, such as Otsuka-Long-Evans-Tokushima-Fatty (OLETF) or streptozotocin-treated rats, they reduce urinary albumin excretion and improve glomerular morphology (15,22). Oral admi...

show abstract

Section: Discussionsupporting

confidence: 90%

“…At the end of the incubation period, two major arabinose degradation products, glyoxal and methylglyoxal, for which pure standards are available, were identified and quantitated by HPLC (28). The standards were used for calibration purposes.…”

Section: Inhibition Of Dicarbonyl Formation By Olmesartanmentioning

confidence: 99%

Angiotensin II Receptor Antagonists and Angiotensin-Converting Enzyme Inhibitors Lower In Vitro the Formation of Advanced Glycation End Products

Miyata¹,

Strihou²,

Ueda³

et al. 2002

Journal of the American Society of Nephrology

Self Cite

282

218

View full text Add to dashboard Cite

show abstract

“…Several in vitro studies have suggested that the presence of several aldehydes and 1,2-dicarbonyl compounds is partly responsible for the cytotoxicity of these fluids [8,9]; however, we have previously demonstrated a minor effect of GDPs on morphological/cellular alterations of the peritoneum in vivo [4]. GDPs can also promote the irreversible formation of advanced glycation end products (AGEs), which in turn can potentially contribute to the toxicity of PD fluids [10]. There is considerable evidence suggesting cytotoxic effects of lactate as the common buffer used in the conventional PD fluids [11].…”

Section: Introductionmentioning

confidence: 81%

Improved biocompatibility of bicarbonate/lactate-buffered PDF is not related to pH

Zareie¹,

Keuning²,

Wee³

et al. 2005

Nephrology Dialysis Transplantation

View full text Add to dashboard Cite

show abstract

“…A growing body of evidence indicates increased concentration of malondialdehyde, a byproduct of the peroxidation of polyunsaturated fatty acids, in plasma and erythrocytes of CPD patients (11,21,22). It has also been shown that plasma levels of advanced glycation end products and advanced oxidation products of proteins are increased in CPD patients compared with healthy subjects (23,24). In contrast to lipids, sugars, and proteins, the reactions of DNA with various oxidants have not been well studied in CPD patients.…”

mentioning

confidence: 99%

Increased Oxidative Damage to Peripheral Blood Leukocyte DNA in Chronic Peritoneal Dialysis Patients

Tarng

Chen

Huang

et al. 2002

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Abstract. This study focuses on the extent of oxidative DNA damage in peripheral blood leukocytes of chronic peritoneal dialysis (CPD) patients. 8-Hydroxy 2'-deoxyguanosine (8-OHdG) contents in peripheral leukocyte DNA were measured by an HPLC-electrochemical detection method in 24 age-and sex-matched healthy subjects, 22 nondialyzed patients with advanced renal failure, and 42 CPD patients. Mean 8-OHdG content was the highest in CPD patients, followed by the nondialyzed patients, and then by the healthy subjects (19.4 versus 11.9 versus 8.3/10 6 dG; ANOVA P Ͻ 0.001). In nondialyzed subjects, peripheral leukocyte 8-OHdG contents inversely correlated with renal creatinine clearance (r ϭ Ϫ0.772; P Ͻ 0.001). Deficiency of blood antioxidants in CPD and nondialyzed patients was expressed by the lower plasma levels of ascorbate, cholesterol-standardized ␣-tocopherol and whole-blood reduced glutathione, and the higher levels of whole-blood oxidized glutathione as compared with healthy subjects (ANOVA P Ͻ 0.05). Mean serum ferritin and iron levels and transferrin saturation were higher in the CPD patients than those in the nondialyzed patients and controls (ANOVA P Ͻ 0.05). Flow cytometric analyses of intracellular reactive oxygen species production of peripheral leukocytes showed that spontaneous production by granulocytes, as well as phorbol-12-myristate-13-acetate (PMA)-induced production by granulocytes, lymphocytes and monocytes, were the highest from CPD patients, followed by nondialyzed patients, and then by the healthy subjects (ANOVA P Ͻ 0.05). Forward stepwise multiple regression disclosed that uremia, PD treatment, spontaneous and PMA-induced reactive oxygen species production in leukocytes, and serum iron were the independent determinants of peripheral leukocyte 8-OHdG content (R 2 ϭ 0.769; P Ͻ 0.001). In conclusion, profound increased 8-OHdG levels in peripheral leukocyte DNA occur in the course of chronic renal failure, gradually increase with its progression, and are further exacerbated by PD treatment.

show abstract

Advanced glycation and lipidoxidation of the peritoneal membrane: Respective roles of serum and peritoneal fluid reactive carbonyl compounds

Abstract: Protein modification of the peritoneum is determined not only by RCOs originating in PD fluid, but also by RCOs originating from the uremic circulation. The present data might be relevant to current attempts to improve PD fluid toxicity by lowering its glucose content.

Cited by 123 publications

References 31 publications

Angiotensin II Receptor Antagonists and Angiotensin-Converting Enzyme Inhibitors Lower In Vitro the Formation of Advanced Glycation End Products

Angiotensin II Receptor Antagonists and Angiotensin-Converting Enzyme Inhibitors Lower In Vitro the Formation of Advanced Glycation End Products

Improved biocompatibility of bicarbonate/lactate-buffered PDF is not related to pH

Increased Oxidative Damage to Peripheral Blood Leukocyte DNA in Chronic Peritoneal Dialysis Patients

Contact Info

Product

Resources

About