Feed-Back Inhibition of Oxidative Stress by Oxidized Lipid/Amino Acid Reaction Products†

Biochemistry ◽  
1997 ◽  
Vol 36 (50) ◽  
pp. 15765-15771 ◽  
Author(s):  
Rosario Zamora ◽  
Manuel Alaiz ◽  
Francisco J. Hidalgo
Keyword(s):  
Oxidative Stress ◽  
Amino Acid ◽  
Reaction Products ◽  
Acid Reaction

Interactions ofStreptomyces griseus aminopeptidase with amino acid reaction products and their implications toward a catalytic mechanism

2001 ◽  
Vol 44 (4) ◽  
pp. 490-504 ◽  
Author(s):  
R. Gilboa ◽  
A. Spungin-Bialik ◽  
G. Wohlfahrt ◽  
D. Schomburg ◽  
S. Blumberg ◽  
...  
Keyword(s):  
Amino Acid ◽  
Catalytic Mechanism ◽  
Reaction Products ◽  
Acid Reaction

Effect of Oxidized Lipid/Amino Acid Reaction Products on the Antioxidative Activity of Common Antioxidants

1998 ◽  
Vol 46 (9) ◽  
pp. 3768-3771 ◽  
Author(s):  
Ishtiaque Ahmad ◽  
Manuel Alaiz ◽  
Rosario Zamora ◽  
Francisco J. Hidalgo
Keyword(s):  
Amino Acid ◽  
Antioxidative Activity ◽  
Reaction Products ◽  
Acid Reaction

Addition of Oxidized Lipid/Amino Acid Reaction Products Delays the Peroxidation Initiated in a Soybean Oil

1995 ◽  
Vol 43 (10) ◽  
pp. 2698-2701 ◽  
Author(s):  
Manuel Alaiz ◽  
Rosario Zamora ◽  
Francisco J. Hidalgo
Keyword(s):  
Amino Acid ◽  
Soybean Oil ◽  
Reaction Products ◽  
Acid Reaction

scholarly journals Amino Acid and Acylcarnitine Levels in Chronic Patients with Schizophrenia: A Preliminary Study

Metabolites ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 34
Author(s):  
Irina A. Mednova ◽  
Alexander A. Chernonosov ◽  
Marat F. Kasakin ◽  
Elena G. Kornetova ◽  
Arkadiy V. Semke ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amino Acids ◽  
Amino Acid ◽  
Chronic Schizophrenia ◽  
Integrated Approach ◽  
Serum Levels ◽  
Tandem Mass ◽  
Chronic Patients ◽  
Healthy Donors ◽  
Preliminary Study

Amino acids and acylcarnitines play an important role as substrates and intermediate products in most of pathways involved in schizophrenia development such as mitochondrial dysfunction, inflammation, lipid oxidation, DNA damage, oxidative stress, and apoptosis. It seems relevant to use an integrated approach with ‘omics’ technology to study their contribution. The aim of our study was to investigate serum amino acid and acylcarnitine levels in antipsychotics-treated patients with chronic schizophrenia compared with healthy donors. We measured serum levels of 15 amino acids and 30 acylcarnitines in 37 patients with schizophrenia and 36 healthy donors by means of tandem mass spectrometry. In summary, patients with chronic schizophrenia had an altered concentration of a few amino acids and acylcarnitines in comparison to the healthy probands. Further research is needed to assess and understand the identified changes.

scholarly journals Amino Acid Transporter LAT1 (SLC7A5) Mediates MeHg-Induced Oxidative Stress Defense in the Human Placental Cell Line HTR-8/SVneo

2021 ◽  
Vol 22 (4) ◽  
pp. 1707
Author(s):  
Sebastian Granitzer ◽  
Raimund Widhalm ◽  
Martin Forsthuber ◽  
Isabella Ellinger ◽  
Gernot Desoye ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amino Acid ◽  
De Novo ◽  
Structural Similarity ◽  
Amino Acid Transporter ◽  
Cell Number ◽  
Mehg Exposure ◽  
Acid Transporter ◽  
And Oxidative Stress

The placental barrier can protect the fetus from contact with harmful substances. The potent neurotoxin methylmercury (MeHg), however, is very efficiently transported across the placenta. Our previous data suggested that L-type amino acid transporter (LAT)1 is involved in placental MeHg uptake, accepting MeHg-L-cysteine conjugates as substrate due to structural similarity to methionine. The aim of the present study was to investigate the antioxidant defense of placental cells to MeHg exposure and the role of LAT1 in this response. When trophoblast-derived HTR-8/SVneo cells were LAT1 depleted by siRNA-mediated knockdown, they accumulated less MeHg. However, they were more susceptible to MeHg-induced toxicity. This was evidenced in decreased cell viability at a usually noncytotoxic concentration of 0.03 µM MeHg (~6 µg/L). Treatment with ≥0.3 µM MeHg increased cytotoxicity, apoptosis rate, and oxidative stress of HTR-8/SVneo cells. These effects were enhanced under LAT1 knockdown. Reduced cell number was seen when MeHg-exposed cells were cultured in medium low in cysteine, a constituent of the tripeptide glutathione (GSH). Because LAT1-deficient HTR-8/SVneo cells have lower GSH levels than control cells (independent of MeHg treatment), we conclude that LAT1 is essential for de novo synthesis of GSH, required to counteract oxidative stress. Genetic predisposition to decreased LAT1 function combined with MeHg exposure could increase the risk of placental damage.

scholarly journals Effects of glutamine supplementation on oxidative stress-related gene expression and antioxidant properties in rats with streptozotocin-induced type 2 diabetes

2011 ◽  
Vol 107 (8) ◽  
pp. 1112-1118 ◽  
Author(s):  
Pei-Hsuan Tsai ◽  
Jun-Jen Liu ◽  
Chui-Li Yeh ◽  
Wan-Chun Chiu ◽  
Sung-Ling Yeh
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Amino Acid ◽  
Oxidative Damage ◽  
Antioxidant Capacity ◽  
Enzyme Activities ◽  
Antioxidant Enzyme Activities ◽  
Related Gene ◽  
Gene Expressions ◽  
Oxidative Stress Related Gene

There are close links among hyperglycaemia, oxidative stress and diabetic complications. Glutamine (GLN) is an amino acid with immunomodulatory properties. The present study investigated the effect of dietary GLN on oxidative stress-relative gene expressions and tissue oxidative damage in diabetes. There were one normal control (NC) and two diabetic groups in the present study. Diabetes was induced by an intraperitoneal injection of nicotinamide followed by streptozotocin (STZ). Rats in the NC group were fed a regular chow diet. In the two diabetic groups, one group (diabetes mellitus, DM) was fed a common semi-purified diet while the other group received a diet in which part of the casein was replaced by GLN (DM-GLN). GLN provided 25 % of total amino acid N. The experimental groups were fed the respective diets for 8 weeks, and then the rats were killed for further analysis. The results showed that blood thioredoxin-interacting protein (Txnip) mRNA expression in the diabetic groups was higher than that in the NC group. Compared with the DM group, the DM-GLN group had lower glutamine fructose-6-phosphate transaminase 1, a receptor of advanced glycation end products, and Txnip gene expressions in blood mononuclear cells. The total antioxidant capacity was lower and antioxidant enzyme activities were altered by the diabetic condition. GLN supplementation increased antioxidant capacity and normalised antioxidant enzyme activities. Also, the renal nitrotyrosine level and Txnip mRNA expression were lower when GLN was administered. These results suggest that dietary GLN supplementation decreases oxidative stress-related gene expression, increases the antioxidant potential and may consequently attenuate renal oxidative damage in rats with STZ-induced diabetes.

Sign in / Sign up

Export Citation Format

Share Document