Preventive aspirin treatment of streptozotocin induced diabetes: blockage of oxidative status and revertion of heme enzymes inhibition

Caballero, Fabiana; Gerez, Esther Noemí; Batlle, Alcira; Vázquez, Elba S.

doi:10.1016/s0009-2797(00)00168-x

Cited by 42 publications

(32 citation statements)

References 30 publications

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“…More recent clinical studies report that T2-diabetic patients showed a 40 mg/dl decrease in fasting plasma glucose levels and a 21% reduction in blood glucose levels during a mixedmeal tolerance test after only 2 weeks of aspirin treatment [38]. Additionally, diabetic rodents treated with aspirin for a short term (7 days) or long-term (45 days to 5 months) regimes display significantly decreased blood glucose and HbA1c levels, similar to our findings [39,49,50]. In contrast, a small clinical study showed that neither aspirin treatment nor ibuprofen reduced fasting blood glucose levels in T2-diabetic patients, however this study had a small number of subjects compared to other studies, making their results difficult to draw conclusions from [54].…”

Section: Resultssupporting

confidence: 89%

Low Dose Aspirin Therapy Decreases Blood Glucose Levels but Does not Prevent Type I Diabetes-induced Bone Loss

Coe

Denison

McCabe

2011

Cell Physiol Biochem

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Backgroud: Diabetes is strongly associated with increased fracture risk. During T1-diabetes onset, levels of blood glucose and pro-inflammatory cytokines (including TNFα) are increased. At the same time, levels of osteoblast markers are rapidly decreased and stay decreased 40 days later at which point bone loss is clearly evident. Inflammation is known to suppress bone formation and induce bone loss. Previous co-culture studies indicate that diabetic bone is inflamed and diabetic bone marrow is capable of enhancing osteoblast death in vitro. Here we investigate a commonly used non-steroidal anti-inflammatory drug, aspirin, to prevent T1-diabetic bone loss in vivo. Methods: We induced diabetes in 16-week-old male C57BL/6 mice and administered aspirin in the drinking water. Results: Our results demonstrate that aspirin therapy reduced diabetic mouse non-fasting blood glucose levels to less than 400 mg/dl, but did not prevent trabecular and cortical bone loss. In control mice, aspirin treatment increased bone formation markers but did not affect markers of bone resorption or bone density/volume. In diabetic mice, bone formation markers and bone density/volume are decreased and unaltered by aspirin treatment. Bone resorption markers, however, are increased and 2-way ANOVA analysis demonstrates an interaction between aspirin treatment and diabetes (p<0.007). Aspirin treatment did not prevent the previously reported diabetes-induced marrow adiposity. Conclusion: Taken together, our results suggest that low dose aspirin therapy does not negatively impact bone density in control and diabetic mice, but could potentially increase bone resorption in T1-diabetic mice.

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Section: Resultssupporting

confidence: 89%

Low Dose Aspirin Therapy Decreases Blood Glucose Levels but Does not Prevent Type I Diabetes-induced Bone Loss

Coe

Denison

McCabe

2011

Cell Physiol Biochem

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“…Preventing the formation of hydroxyl radicals would be an efficient means to reduce hydroxylinduced damage, and several compounds have been tested as antioxidants in diabetic animals with varying success. For example, the increase in TBARS associated with diabetes is prevented by treatment with nicotinamide [61], boldine [62], melatonin [45,49,63], aspirin [74], L-arginine or sodium nitroprusside [67], probucol [51], ␣-lipoic acid [71,77], aminoguanidine [69], captopril, enalapril [65], or nitecapone [66], if this treatment is given before or immediately after the diabetogen.…”

Section: Lipid Peroxidationmentioning

confidence: 99%

“…These normalization effects are seen in kidney [58,59,62,65,66,78], liver [58][59][60][61][62]64,74], heart [51][52][53]77], brain [49], intestine [58], lung [60], pancreas [45,61,62], Diabetogens alloxan (ALX) or streptozotocin (STZ), administered to mice or Wistar or Sprague-Dawley (SD) rats, produced increases (⇑) or decreases (⇓) from normal levels of TBARS as indicated in the top line for each study. Dose and route of diabetogen administration is indicated in the second line of column 2, and the asterisk in line 3 indicates diabetogen treatment continued for the specified number of days.…”

Section: Lipid Peroxidationmentioning

confidence: 99%

Diabetes, oxidative stress, and antioxidants: A review

Maritim

Sanders

Watkins

2003

J Biochem & Molecular Tox

2,668

1,801

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Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of both types of diabetes mellitus. Free radicals are formed disproportionately in diabetes by glucose oxidation, nonenzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation, and development of insulin resistance. These consequences of oxidative stress can promote the development of complications of diabetes mellitus. Changes in oxidative stress biomarkers, including superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, glutathione levels, vitamins, lipid peroxidation, nitrite concentration, nonenzymatic glycosylated proteins, and hyperglycemia in diabetes, and their consequences, are discussed in this review. In vivo studies of the effects of various conventional and alternative drugs on these biomarkers are surveyed. There is a need to continue to explore the relationship between free radicals, diabetes, and its complications, and to elucidate the mechanisms by which increased oxidative stress accelerates the development of diabetic complications, in an effort to expand treatment options.

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“…For example, aspirin (acetylsalicylic acid) is known to inhibit glycation by acetylating free amino groups of a protein, thereby blocking the attachment of reducing sugars (Caballero et al 2000;Malik and Meek 1994) at the early stage of the glycation process. The inhibitory activities against AGE formation of various vitamin B1 and B6 derivatives such as pyridoxamine (Khalifah et al 1999;Metz et al 2003;Voziyan et al 2002) and thiamine pyrophosphate (Booth et al 1997) have mainly been attributed to their abilities to scavenge reactive carbonyl compounds (Ahmed et al 2005a;Voziyan et al 2002).…”

Section: Anti-age Therapiesmentioning

confidence: 99%

Advanced glycation End-products (AGEs): an emerging concern for processed food industries

et al. 2015

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The global food industry is expected to increase more than US $ 7 trillion by 2014. This rise in processed food sector shows that more and more people are diverging towards modern processed foods. As modern diets are largely heat processed, they are more prone to contain high levels of advanced glycation end products (AGEs). AGEs are a group of complex and heterogeneous compounds which are known as brown and fluorescent cross-linking substances such as pentosidine, non-fluorescent cross-linking products such as methylglyoxal-lysine dimers (MOLD), or non-fluorescent, non-cross linking adducts such as carboxymethyllysine (CML) and pyrraline (a pyrrole aldehyde). The chemistry of the AGEs formation, absorption and bioavailability and their patho-biochemistry particularly in relation to different complications like diabetes and ageing discussed. The concept of AGEs receptor -RAGE is mentioned. AGEs contribute to a variety of microvascular and macrovascular complications through the formation of cross-links between molecules in the basement membrane of the extracellular matrix and by engaging the receptor for advanced glycation end products (RAGE). Different methods of detection and quantification along with types of agents used for the treatment of AGEs are reviewed. Generally, ELISA or LC-MS methods are used for analysis of foods and body fluids, however lack of universally established method highlighted. The inhibitory effect of bioactive components on AGEs by trapping variety of chemical moieties discussed. The emerging evidence about the adverse effects of AGEs makes it necessary to investigate the different therapies to inhibit AGEs.

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Preventive aspirin treatment of streptozotocin induced diabetes: blockage of oxidative status and revertion of heme enzymes inhibition

Cited by 42 publications

References 30 publications

Low Dose Aspirin Therapy Decreases Blood Glucose Levels but Does not Prevent Type I Diabetes-induced Bone Loss

Low Dose Aspirin Therapy Decreases Blood Glucose Levels but Does not Prevent Type I Diabetes-induced Bone Loss

Diabetes, oxidative stress, and antioxidants: A review

Advanced glycation End-products (AGEs): an emerging concern for processed food industries

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