The Effect of N-Acetylcysteine on Respiratory Enzymes, ADP/ATP Ratio, Glutathione Metabolism, and Nitrosative Stress in the Salivary Gland Mitochondria of Insulin Resistant Rats

Zalewska, Anna; Szarmach, Izabela; Żendzian-Piotrowska, Małgorzata

doi:10.3390/nu12020458

Cited by 25 publications

(32 citation statements)

References 71 publications

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“…Due to structural similarity, both AGEs and AOPPs combine with a specific receptor (RAGE) to stimulate the proinflammatory NFkB signaling pathway [ 13 , 49 , 50 ]. Its activation not only increases the production of cytokines and chemokines, but also results in increased secretion of prothrombotic factors and oxygen free radicals [ 13 , 50 , 51 ]. Interestingly, protein glyco-oxidation is not only intensified under metabolic disturbances (e.g., oxidative stress, hyperglycemia, insulin resistance, diabetes mellitus or abnormal lipid metabolism).…”

Section: Discussionmentioning

confidence: 99%

A New Insight into Meloxicam: Assessment of Antioxidant and Anti-Glycating Activity in In Vitro Studies

et al. 2020

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Meloxicam is a non-steroidal anti-inflammatory drug, which has a preferential inhibitory effect to cyclooxyganase-2 (COX-2). Although the drug inhibits prostaglandin synthesis, the exact mechanism of meloxicam is still unknown. This is the first study to assess the effect of meloxicam on protein glyco-oxidation as well as antioxidant activity. For this purpose, we used an in vitro model of oxidized bovine serum albumin (BSA). Glucose, fructose, ribose, glyoxal and methylglyoxal were used as glycating agents, while chloramine T was used as an oxidant. We evaluated the antioxidant properties of albumin (2,2-di-phenyl-1-picrylhydrazyl radical scavenging capacity, total antioxidant capacity and ferric reducing antioxidant power), the intensity of protein glycation (Amadori products, advanced glycation end products) and glyco-oxidation (dityrosine, kynurenine, N-formylkynurenine, tryptophan and amyloid-β) as well as the content of protein oxidation products (advanced oxidation protein products, carbonyl groups and thiol groups). We have demonstrated that meloxicam enhances the antioxidant properties of albumin and prevents the protein oxidation and glycation under the influence of various factors such as sugars, aldehydes and oxidants. Importantly, the antioxidant and anti-glycating activity is similar to that of routinely used antioxidants such as captopril, Trolox, reduced glutathione and lipoic acid as well as protein glycation inhibitors (aminoguanidine). Pleiotropic action of meloxicam may increase the effectiveness of anti-inflammatory treatment in diseases with oxidative stress etiology.

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Section: Discussionmentioning

confidence: 99%

A New Insight into Meloxicam: Assessment of Antioxidant and Anti-Glycating Activity in In Vitro Studies

et al. 2020

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“…The GSH concentration was calculated using the difference between the levels of total glutathione and GSSG. Redox (oxidation/reduction) status was calculated using the formula [GSH] 2 /[GSSG] [ 28 ]. The thiol group concentration was colorimetrically measured using Ellman’s reagent (DTNB) in 0.1 M phosphate buffer, pH 8.0 [ 29 ].…”

Section: Methodsmentioning

confidence: 99%

High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis

et al. 2020

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Despite several reports on the relationship between metabolic and neurodegenerative diseases, the effect of a high-sugar diet (HSD) on brain function is still unknown. Given the crucial role of oxidative stress in the pathogenesis of these disorders, this study was the first to compare the effect of an HSD on the activity of prooxidative enzymes, enzymatic and non-enzymatic antioxidants, and protein oxidative damage in the brain structures regulating energy metabolism (hypothalamus) and cognitive functions (cerebral cortex). Male Wistar rats were randomly divided into two groups (n = 10)—control diet (CD) and high-sugar diet (HSD)—for 8 weeks. We showed a decrease in glutathione peroxidase and superoxide dismutase activity and an increase in catalase activity in the hypothalamus of HSD rats compared to controls. The activity of xanthine oxidase and NADPH oxidase and the contents of oxidation (protein carbonyls), glycoxidation (dityrosine, kynurenine and N-formylkynurenine) and protein glycation products (advanced glycation end products and Amadori products) were significantly higher only in the hypothalamus of the study group. The HSD was also responsible for the disruption of antioxidant systems and oxidative damage to blood proteins, but we did not show any correlation between systemic redox homeostasis and the brain levels. In summary, HSD is responsible for disorders of enzymatic antioxidant defenses only at the central (plasma/serum) and hypothalamic levels but does not affect the cerebral cortex. The hypothalamus is much more sensitive to oxidative damage caused by an HSD than the cerebral cortex.

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“…In our study, the severity of protein oxidation (↑PC and ↓total thiols) and glycoxidation (↑dityrosine, ↑kynurenine, ↑ N -formylkynurenine, and ↓tryptophan) was significantly higher in NWS of stroke patients with hyposalivation compared to the control group. Products of protein oxidation/glycation can aggregate and accumulate in the salivary glands, leading to impaired secretory function and thus changes in saliva composition [ 14 , 17 – 19 ]. This hypothesis may be confirmed by strong correlations between oxidation/protein glycation products and salivary flow rate, total protein content, and salivary amylase activity.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulation of such products as deposits may cause stiffening of the salivary glands' blood vessels/secretory cells. Furthermore, in these conditions, extracellular matrix hypertrophy can also occur [ 14 , 17 – 19 , 25 ]. Since it is ethically impossible to collect salivary gland samples from stroke patients with hyposalivation, further studies on an animal model are necessary to confirm our hypotheses.…”

Section: Discussionmentioning

confidence: 99%

“…This hypothesis is likely since oxidative stress is the primary factor damaging the salivary glands in both oral and systemic diseases [ 15 , 16 ]. Indeed, protein glycoxidation products can aggregate and accumulate in the salivary glands leading to morphological changes and qualitative and quantitative disorders of saliva secretion [ 17 – 19 ]. However, of all cellular biomolecules, proteins are believed to be the primary target of ROS attack [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

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Salivary Gland Dysfunction in Stroke Patients Is Associated with Increased Protein Glycoxidation and Nitrosative Stress

Maciejczyk

Gerreth²,

Hojan

et al. 2020

Oxidative Medicine and Cellular Longevity

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Stroke is one of the leading causes of disability and death worldwide. Despite intensive medical care, many of the complaints directly threatening the patient’s life marginalize their dental needs after the stroke. Recent studies indicate reduced saliva secretion in stroke patients in addition to the increased incidence of caries and periodontal disease. Since oxidative stress plays a vital role in the pathogenesis of salivary gland hypofunction and neurodegenerative disorders (including stroke), this is the first to evaluate the relationship between salivary gland activity and protein glycoxidation and nitrosative damage. The content of glycation and protein oxidation products and nitrosative stress was assessed in nonstimulated (NWS) and stimulated (SWS) whole saliva of stroke patients with normal salivary secretion and hyposalivation (reduced saliva production). The study included 30 patients in the stroke’s subacute phase and 30 healthy controls matched by age and sex. We have shown that stroke patients with hyposalivation show increased contents of protein glycation (↑Amadori products and ↑advanced glycation end products), glycoxidation (↑dityrosine), and nitration (↑nitrotyrosine) products compared to stroke cases with normal salivary secretion and control group. Interestingly, higher oxidative/nitrosative stress was found in NWS, which strongly correlates with salivary flow rate, total protein content, and salivary amylase activity. Such relationships were not observed in the control group. Summarizing, oxidative and nitrosative stress may be one of the mechanisms responsible for the impairment of saliva secretion in stroke patients. However, extraglandular sources of salivary oxidative stress in stroke patients cannot be excluded. Further studies to assess salivary gland hypofunction in stroke cases are necessary.

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The Effect of N-Acetylcysteine on Respiratory Enzymes, ADP/ATP Ratio, Glutathione Metabolism, and Nitrosative Stress in the Salivary Gland Mitochondria of Insulin Resistant Rats

Cited by 25 publications

References 71 publications

A New Insight into Meloxicam: Assessment of Antioxidant and Anti-Glycating Activity in In Vitro Studies

A New Insight into Meloxicam: Assessment of Antioxidant and Anti-Glycating Activity in In Vitro Studies

High-Sugar Diet Disrupts Hypothalamic but Not Cerebral Cortex Redox Homeostasis

Salivary Gland Dysfunction in Stroke Patients Is Associated with Increased Protein Glycoxidation and Nitrosative Stress

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