scholarly journals Influence of the butylparaben administration on the oxidative stress metabolism of liver, kidney and spleen

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Duygu Aydemir ◽  
Burcu Oztasci ◽  
Nurhayat Barlas ◽  
Nuriye Nuray Ulusu
Keyword(s):  
Oxidative Stress ◽  
Enzyme Activities ◽  
Pentose Phosphate ◽  
The Body ◽  
Male Rats ◽  
Published Data ◽  
Antioxidant Enzyme Activities ◽  
Glutathione S Transferase ◽  
Glucose Phosphate ◽  
Liver And Kidney

AbstractObjectivesButylparaben is widely used synthetic polymer as preservative in the food, pharmaceutical and cosmetic industries. Although butylparaben is metabolized in the detoxification organs including liver and kidney, some parts of it can retain and accumulate in the body. Parabens can impair developmental and reproductive health, though there is not any published data related with the influence of the butylparaben on the oxidative stress metabolism in the detoxification organs. Therefore, we aimed to evaluate antioxidant enzyme activities in the liver, kidney and spleen of butylparaben-treated rat.MethodsPrepubertal Wistar albino male rats were administered with 0, 100, 200, 400 mg/kg/day butylparaben for 28 days. After treatment, enzyme activities were evaluated as the biomarkers of the oxidative stress.ResultsEnzyme activities including glucose-phosphate dehydrogenase (G6PD), 6-phosphoglucanate dehydrogenase (6-PGD), glutathione reductase (GR), glutathione s-transferase (GST) and glutathione peroxidase (GPx) were impaired upon butylparaben treatment in the liver, kidney and spleen tissues.ConclusionsExposure to endocrine disruptors may affect enzyme activities of the detoxification organs and change the pentose phosphate glutathione (GSH) metabolisms. According to our data oxidative stress metabolism is impaired in the spleen, kidney and liver tissue upon butylparaben treatment that has been indicated first time in the literature.

Potential protective effects of the edible alga Arthrospira platensis against lead-induced oxidative stress, anemia, kidney injury, and histopathological changes in adult rats

2019 ◽  
Vol 44 (3) ◽  
pp. 271-281 ◽  
Author(s):  
Manel Gargouri ◽  
Ahlem Soussi ◽  
Amel Akrouti ◽  
Christian Magné ◽  
Abdelfattah El Feki
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Hematological Parameters ◽  
Kidney Injury ◽  
Arthrospira Platensis ◽  
Male Rats ◽  
Antioxidant Enzyme Activities ◽  
Protein Carbonyl Content

Oxidative damage has been proposed as a possible mechanism involved in lead toxicity. This study investigated the possible protective effect of dietary Arthrospira platensis supplementation against lead acetate-induced kidney injury in adult male rats. Rats were divided into 4 groups: normal rats (control rats), rats treated with spirulina, rats treated with lead (Pb) (0.344 g/kg body weight), and rats treated with Pb and spirulina. The exposure of rats to Pb for 30 days provoked renal damage with significant increases in hematological parameters, oxidative stress-related parameters (i.e., thiobarbituric acid reactive substances, protein carbonyl content, advanced oxidation protein products, and hydrogen peroxide), creatinine and urea levels in plasma, and uric acid level in urine. Conversely, antioxidant enzyme activities (i.e., catalase, glutathione peroxidase, and superoxide dismutase) and levels of nonprotein thiols, plasma uric acid, and urinary creatinine and urea decreased. The administration of spirulina to Pb-treated rats significantly improved weight, peripheral blood parameters, oxidative stress-related parameters, renal biomarker levels, and antioxidant enzyme activities. Also, rats treated with Pb and spirulina had normal kidney histology. These healing effects are likely the result of the high phenol content and significant antioxidant capacity of A. platensis. Our data strongly suggest that spirulina supplementation improves kidney function and plays an important role in the prevention of complications of Pb intoxication.

scholarly journals Consumption of Anacardium occidentale L. (Cashew Nuts) Inhibits Oxidative Stress through Modulation of the Nrf2/HO−1 and NF-kB Pathways

Molecules ◽  
2020 ◽  
Vol 25 (19) ◽  
pp. 4426
Author(s):  
Roberta Fusco ◽  
Marika Cordaro ◽  
Rosalba Siracusa ◽  
Alessio Filippo Peritore ◽  
Enrico Gugliandolo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superior Mesenteric Artery ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Mesenteric Artery ◽  
Ischemia Reperfusion ◽  
Anacardium Occidentale ◽  
Male Rats ◽  
Antioxidant Enzyme Activities ◽  
Myeloperoxidase Activity

Ischemia/reperfusion injury is a severe disorder associated with a high mortality. Several antioxidant and pharmacological properties of cashew nuts (Anacardium occidentale L.) and its metabolites from different countries have recently been described. It is a medicinal plant with important therapeutic effects. This study aimed to verify the effect of an oral administration of cashew nuts in a rat model of ischemia/reperfusion (I/R). Adult male rats were subjected to intestinal I/R injury by clamping the superior mesenteric artery for 30 min and then allowing animals to 1 h of reperfusion. Rats subjected to I/R of the gut showed a significant increase in different biochemical markers. In particular, we evaluated lipid peroxidation, tissue myeloperoxidase activity, protein carbonyl content, reactive oxygen species generation and decreased antioxidant enzyme activities. Western blot analysis showed the activation of the NRF2 and NF-kB pathways. Increased immunoreactivity to nitrotyrosine, PARP, P-selectin, and ICAM-1 was observed in the ileum of rats subjected to I/R. Administration of cashew nuts (100 mg/kg) significantly reduced the mortality rate, the fall in arterial blood pressure, and oxidative stress and restored the antioxidant enzyme activities by a mechanism involving both NRF2 and NF-kB pathways. Cashew nuts treatments reduced cytokines plasma levels, nitrotyrosine, and PARP expression as well as adhesion molecules expressions. Additionally, cashew nuts decreased the intestinal barrier dysfunction and mucosal damage, the translocation of toxins and bacteria, which leads to systemic inflammation and associated organs injuries in particular of liver and kidney. Our study demonstrates that cashew nuts administration exerts antioxidant and pharmacological protective effects in superior mesenteric artery occlusion–reperfusion shock.

scholarly journals Coenzyme Q10 and Silymarin Reduce CCl4-Induced Oxidative Stress and Liver and Kidney Injury in Ovariectomized Rats—Implications for Protective Therapy in Chronic Liver and Kidney Diseases

2021 ◽  
Vol 28 (1) ◽  
pp. 50-63 ◽  
Author(s):  
Samanta Sifat Lamia ◽  
Tushar Emran ◽  
Jubaida Khatun Rikta ◽  
Nowreen Islam Chowdhury ◽  
Manoneeta Sarker ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzyme ◽  
Coenzyme Q10 ◽  
Enzyme Activities ◽  
Kidney Diseases ◽  
Inflammatory Cells ◽  
Chronic Liver ◽  
Ovariectomized Rats ◽  
Antioxidant Enzyme Activities ◽  
Liver And Kidney

Oxidative stress is one of the key factors in the pathophysiology of liver disease. The present study aimed to evaluate the potential impact of two antioxidants, namely coenzyme Q10 (CoQ10) and silymarin, on carbon tetrachloride (CCl4)-induced oxidative stress and hepatic damage in ovariectomized rats. Female Long Evans rats were divided into six groups (n = 6): control, CCl4, CCl4 + CoQ10 (200 mg/kg), CCl4 + silymarin (140 mg/kg), Control + CoQ10, and Control + silymarin. Plasma and tissues from liver and kidney were analyzed for oxidative stress parameters and antioxidant enzyme activities using biochemical assays. Infiltration of inflammatory cells and fibrosis were assessed by histological staining of tissue sections. Both CoQ10 and silymarin significantly lowered serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) levels that were detected to be higher in CCl4 rats compared to controls. Significant reduction in CCl4-induced elevated levels of oxidative stress markers malondialdehyde (MDA), nitric oxide (NO), and advanced protein oxidation product (APOP) was observed with both antioxidants. However, in control rats, CoQ10 and silymarin did not produce a significant effect. Histological analysis revealed that CCl4 markedly increased the level of inflammatory cells infiltration and fibrosis in liver and kidney tissues, but this was significantly reduced in CCl4 + CoQ10 and CCl4 + silymarin groups. Taken together, our results suggest that CoQ10 and silymarin can protect the liver against oxidative damage through improved antioxidant enzyme activities and reduced lipid peroxidation. Thus, supplementation of the aforementioned antioxidants may be useful as a therapeutic intervention to protect liver health in chronic liver diseases.

scholarly journals Effects of butylparaben on antioxidant enzyme activities and histopathological changes in rat tissues

2019 ◽  
Vol 70 (4) ◽  
pp. 315-324
Author(s):  
Duygu Aydemir ◽  
Burcu Öztaşcı ◽  
Nurhayat Barlas ◽  
Nuriye Nuray Ulusu
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzyme ◽  
Tissue Damage ◽  
Enzyme Activities ◽  
Corn Oil ◽  
Male Rats ◽  
Antioxidant Enzyme Activities ◽  
Rat Tissues ◽  
Histopathological Changes

AbstractButyl p-hydroxybenzoic acid, also known as butylparaben (BP), is one of the most common parabens absorbed by the skin and gastrointestinal tract and metabolised in the liver and kidney. Recent in vivo and in vitro studies have raised concern that BP causes reproductive, development, and teratogenic toxicity. However, BP-induced oxidative stress and its relation to tissue damage has not been widely investigated before. Therefore, we aimed to investigate the effects of butyl 4-hydroxybenzoate on enzyme activities related to the pentose phosphate pathway and on glutathione-dependent enzymes such as glucose 6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6-PGD), glutathione reductase (GR), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) in kidney, liver, brain, and testis tissues. Male rats were randomly divided into four groups to orally receive corn oil (control) or 200, 400, or 800 mg/kg/day of BP for 14 days. Then we measured G6PD, GR, GST, 6-PGD, and GPx enzyme activities in these tissues and studied histopathological changes. BP treatment caused imbalance in antioxidant enzyme activities and tissue damage in the liver, kidney, brain, and testis. These findings are the first to show the degenerative role of BP on the cellular level. The observed impairment of equivalent homeostasis and antioxidant defence points to oxidative stress as a mechanism behind tissue damage caused by BP.

The protective role of luteolin against the methotrexate-induced hepato-renal toxicity via its antioxidative, anti-inflammatory, and anti-apoptotic effects in rats

2021 ◽  
pp. 096032712199190
Author(s):  
AA Dar ◽  
A Fehaid ◽  
S Alkhatani ◽  
S Alarifi ◽  
WS Alqahtani ◽  
...  
Keyword(s):  
Renal Toxicity ◽  
Histopathological Examination ◽  
Protective Role ◽  
Male Rats ◽  
Antioxidant Enzyme Activities ◽  
Serum Samples ◽  
Liver And Kidney ◽  
Anti Inflammatory ◽  
Induced Changes ◽  
Apoptotic Effects

Methotrexate (MTX) is frequently used drug in treatment of cancer and autoimmune diseases. Unfortunately, MTX has many side effects including the hepato-renal toxicity. In this study, we hypothesized that Luteolin (Lut) exhibits protective effect against the MTX-induced hepato-renal toxicity. In order to investigate our hypothesis, the experiment was designed to examine the effect of exposure of male rats to MTX (20 mg/kg, i.p., at day 9) alone or together with Lut (50 mg/kg, oral for 14 days) compared to the control rats (received saline). The findings demonstrated that MTX treatment induced significant increases in the liver and kidney functions markers in serum samples including Aspartate transaminase (AST), Alanine transaminase (ALT), creatinine, urea and uric acid. MTX also mediated an oxidative stress expressed by elevated malondialdehyde (MDA) level and decreased level of reduced glutathione (GSH), antioxidant enzyme activities, and downregulation of the Nrf2 gene expression as an antioxidant trigger. Moreover, the inflammatory markers (NF-κB, TNF-α, and IL-1β) were significantly elevated upon MTX treatment. In addition, MTX showed an apoptotic response mediated by elevating the pro-apoptotic (Bax) and lowering the anti-apoptotic (Bcl-2) proteins. All of these changes were confirmed by the observed alterations in the histopathological examination of the hepatic and renal tissues. Lut exposure significantly reversed all the MTX-induced changes in the measured parameters suggesting its potential protective role against the MTX-induced toxicity. Finally, our findings concluded the antioxidative, anti-inflammatory and anti-apoptotic effects of Lut as a mechanism of its protective role against the MTX-induced hepato-renal toxicity in rats.

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.

scholarly journals Antioxidants and selenocompounds inhibit 3,5-dimethylaminophenol toxicity to human urothelial cells

2019 ◽  
Vol 70 (1) ◽  
pp. 18-29 ◽  
Author(s):  
Pinar Erkekoglu ◽  
Ming-Wei Chao ◽  
Chia-Yi Tseng ◽  
Bevin P. Engelward ◽  
Ozge Kose ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bladder Cancer ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Mammalian Cells ◽  
Antioxidant Enzyme Activities ◽  
Urothelial Cells ◽  
Dna Breaks ◽  
Primary Metabolite ◽  
Stress Changes

AbstractExposure to alkyl anilines may lead to bladder cancer, which is the second most frequent cancer of the urogenital tract. 3,5-dimethylaniline is highly used in industry. Studies on its primary metabolite 3,5-dimethylaminophenol (3,5-DMAP) showed that this compound causes oxidative stress, changes antioxidant enzyme activities, and leads to death of different mammalian cells. However, there is no in vitro study to show the direct effects of 3,5-DMAP on human bladder and urothelial cells. Selenocompounds are suggested to decrease oxidative stress caused by some chemicals, and selenium supplementation was shown to reduce the risk of bladder cancer. The main aim of this study was to investigate whether selenocompounds organic selenomethionine (SM, 10 µmol/L) or inorganic sodium selenite (SS, 30 nmol/L) could reduce oxidative stress, DNA damage, and apoptosis in UROtsa cells exposed to 3,5-DMAP. 3,5-DMAP caused a dose-dependent increase in intracellular generation of reactive oxygen species, and its dose of 50 µmol/L caused lipid peroxidation, protein oxidation, and changes in antioxidant enzyme activities in different cellular fractions. The comet assay also showed single-strand DNA breaks induced by the 3,5-DMAP dose of 50 µmol/L, but no changes in double-strand DNA breaks. Apoptosis was also triggered. Both selenocompounds provided partial protection against the cellular toxicity of 3,5-DMAP. Low selenium status along with exposure to alkyl anilines can be a major factor in the development of bladder cancer. More mechanistic studies are needed to specify the role of selenium in bladder cancer.

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