scholarly journals Effects of microplastic fibers on Lates calcarifer juveniles: Accumulation, oxidative stress, intestine microbiome dysbiosis and histological damage

2021 ◽  
Vol 133 ◽  
pp. 108370
Author(s):  
Mujiao Xie ◽  
Lang Lin ◽  
Peng Xu ◽  
Weiguo Zhou ◽  
Changsheng Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lates Calcarifer ◽  
Histological Damage ◽  
Intestine Microbiome

scholarly journals TIGAR regulates glycolysis in ischemic kidney proximal tubules

2015 ◽  
Vol 308 (4) ◽  
pp. F298-F308 ◽  
Author(s):  
Jinu Kim ◽  
Kishor Devalaraja-Narashimha ◽  
Babu J. Padanilam
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Pentose Phosphate Pathway ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pentose Phosphate ◽  
Atp Depletion ◽  
G6pd Activity ◽  
Histological Damage ◽  
Severe Ischemia

Tp53-induced glycolysis and apoptosis regulator (TIGAR) activation blocks glycolytic ATP synthesis by inhibiting phosphofructokinase-1 activity. Our data indicate that TIGAR is selectively induced and activated in renal outermedullary proximal straight tubules (PSTs) after ischemia-reperfusion injury in a p53-dependent manner. Under severe ischemic conditions, TIGAR expression persisted through 48 h postinjury and induced loss of renal function and histological damage. Furthermore, TIGAR upregulation inhibited phosphofructokinase-1 activity, glucose 6-phosphate dehydrogenase (G6PD) activity, and induced ATP depletion, oxidative stress, autophagy, and apoptosis. Small interfering RNA-mediated TIGAR inhibition prevented the aforementioned malevolent effects and protected the kidneys from functional and histological damage. After mild ischemia, but not severe ischemia, G6PD activity and NADPH levels were restored, suggesting that TIGAR activation may redirect the glycolytic pathway into gluconeogenesis or the pentose phosphate pathway to produce NADPH. The increased level of NADPH maintained the level of GSH to scavenge ROS, resulting in a lower sensitivity of PST cells to injury. Under severe ischemia, G6PD activity and NADPH levels were reduced during reperfusion; however, blockade of TIGAR enhanced their levels and reduced oxidative stress and apoptosis. Collectively, these results demonstrate that inhibition of TIGAR may protect PST cells from energy depletion and apoptotic cell death in the setting of severe ischemia-reperfusion injury. However, under low ischemic burden, TIGAR activation induces the pentose phosphate pathway and autophagy as a protective mechanism.

Mitigation of IL-1β, IL-6, TNF-α, and markers of apoptosis by ursolic acid against cisplatin-induced oxidative stress and nephrotoxicity in rats

2021 ◽  
Vol 40 (12_suppl) ◽  
pp. S397-S405
Author(s):  
Pankaj Tripathi ◽  
Saeed Alshahrani
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Uric Acid ◽  
Inflammatory Cytokines ◽  
Caspase 3 ◽  
Caspase 9 ◽  
Histological Damage ◽  
Tnf Α ◽  
Mda Content ◽  
Pro Inflammatory Cytokines

Background: Ursolic acid (UA) is a natural pentacyclic triterpenoid that is known for its benefits under several pathological conditions. Cisplatin (CP) is among the most preferred chemotherapeutic agents; however, its nephrotoxicity limits its clinical utility. Purpose: This study was aimed to determine the role of UA in the reduction of CP-induced nephrotoxicity and mitigation of pro-inflammatory cytokines and apoptosis in a rat model. Methodology: Male Wistar rats were randomized into vehicle control, CP (7.5 mg/kg), UA 10 mg/kg, and CP with UA 5 and 10 mg/kg groups. Kidney and blood samples were collected for assessment of renal function, measurement of pro-inflammatory cytokines, apoptosis markers, antioxidant activity, and tissue histology. Results: CP significantly increased the levels of serum Cr, BUN, and uric acid; it also induced histological damage reflecting the pathophysiology observed during nephrotoxicity. CP has also shown its pro-oxidant activity in kidney tissue because CP decreased the levels of GSH, SOD, and CAT; it increased the lipid peroxidation as measured by MDA content. In addition, CP significantly upregulated the activity of pro-inflammatory cytokines and expression of apoptotic markers, that is, there were increased levels of IL-1β, IL-6, TNF-α, caspase-3, and caspase-9. Two weeks of continuous treatment of UA showed significant recovery against CP-induced nephrotoxicity; UA decreased the levels of Cr, BUN, and uric acid and ameliorated histological damage. UA also downregulated the activities of IL-1β, IL-6, and TNF-α as well as expression of caspase-3 and caspase-9. Furthermore, CP-induced oxidative stress that was antagonized by UA—the levels of GSH, SOD, and CAT were significantly increased while MDA content was decreased. Conclusions: UA has a protective effect against CP-induced nephrotoxicity, which may be due to its antioxidant activity and mitigation of ILβ-1, ILβ-6, TNF-α, and markers of apoptosis.

scholarly journals Role of Rutin in 5-Fluorouracil-Induced Intestinal Mucositis: Prevention of Histological Damage and Reduction of Inflammation and Oxidative Stress

Molecules ◽  
2020 ◽  
Vol 25 (12) ◽  
pp. 2786
Author(s):  
Lázaro de Sousa Fideles ◽  
João Antônio Leal de Miranda ◽  
Conceição da Silva Martins ◽  
Maria Lucianny Lima Barbosa ◽  
Helder Bindá Pimenta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Mechanisms ◽  
Cell Counts ◽  
Histological Damage ◽  
Inflammatory Processes ◽  
Intestinal Mucositis ◽  
Cox 2 ◽  
And Oxidative Stress ◽  
Immunohistochemical Analyses

Intestinal mucositis, characterized by inflammatory and/or ulcerative processes in the gastrointestinal tract, occurs due to cellular and tissue damage following treatment with 5-fluorouracil (5-FU). Rutin (RUT), a natural flavonoid extracted from Dimorphandra gardneriana, exhibits antioxidant, anti-inflammatory, cytoprotective, and gastroprotective properties. However, the effect of RUT on inflammatory processes in the intestine, especially on mucositis promoted by antineoplastic agents, has not yet been reported. In this study, we investigated the role of RUT on 5-FU-induced experimental intestinal mucositis. Swiss mice were randomly divided into seven groups: Saline, 5-FU, RUT-50, RUT-100, RUT-200, Celecoxib (CLX), and CLX + RUT-200 groups. The mice were weighed daily. After treatment, the animals were euthanized and segments of the small intestine were collected to evaluate histopathological alterations (morphometric analysis); malondialdehyde (MDA), myeloperoxidase (MPO), and glutathione (GSH) concentrations; mast and goblet cell counts; and cyclooxygenase-2 (COX-2) activity, as well as to perform immunohistochemical analyses. RUT treatment (200 mg/kg) prevented 5-FU-induced histopathological changes and reduced oxidative stress by decreasing MDA concentrations and increasing GSH concentrations. RUT attenuated the inflammatory response by decreasing MPO activity, intestinal mastocytosis, and COX-2 expression. These results suggest that the COX-2 pathway is one of the underlying protective mechanisms of RUT against 5-FU-induced intestinal mucositis.

scholarly journals Protective Effect of Hydroalcoholic Extract of Orange Peel on PCNA and FSH-R Gene Expression in Histological Damage and Oxidative Stress Due to Ovarian Torsion in Adult Rats

2021 ◽  
Vol 9 (3) ◽  
pp. 205-211
Author(s):  
Seyedeh-Roza Tafrishi Nejad ◽  
Arash Khaki ◽  
Shamci Abbasalizadeh ◽  
Majid Shokoohi ◽  
Nava Ainehchi
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Protective Effect ◽  
Ovarian Tissue ◽  
Orange Peel ◽  
Ovarian Torsion ◽  
R Gene ◽  
Adult Rats ◽  
Hydroalcoholic Extract ◽  
Histological Damage

Objectives: The aim of this study was to evaluate the protective effect of the hydroalcoholic extract of orange peel on proliferating cell nuclear antigen (PCNA) and follicle-stimulating hormone receptor (FSH-R) gene expression in histological injuries and acid stress caused by ovarian torsion in adult rats. Materials and Methods: In this experimental study, 32 adult female rats were randomly divided into 4 groups. In group 1 (Sham), the abdominal wall was cut without applying torsion and in group 2, ovarian torsion was performed for 2 hours, followed by detorsion for 2 weeks. The hydro-alcoholic extract of orange peel was added to their diet for two weeks in group 3, followed by ovarian torsion for 2 hours and detorsion for 2 hours. Group 4 received the orange peel extract for two weeks and after then ovarian resection for the evaluation of histological damage and blood sampling to examine the serum level of antioxidant enzymes, as well as the expression of PCNA and FSH-R genes in the ovarian tissue. Results: Histological changes in the ovary tissue of rats showed that torsion and detorsion have destructive effects on the ovarian tissue, and torsion/detorsion led to a reduction in the expression of PCNA and FSH-R (P < 0.05). Based on biochemical and hormonal results, the ovarian torsion resulted in an imbalance in the oxidative stress markers and hormone profile of rats. Finally, the administration of the hydroalcoholic extract of orange peel due to its high antioxidant properties improves these effects. Conclusions: In general, administering an appropriate dose of the hydroalcoholic extract of orange peel for two consecutive weeks in the diet had a protective effect on the ovarian tissue at the risk of torsion/detorsion.

scholarly journals Pneumoperitoneum effect on testicular oxidative stress and histopathology – Systematic review

2021 ◽  
Vol 10 (3) ◽  
pp. e13410313069
Author(s):  
Bruno Albuquerque de Almeida ◽  
Vanessa Milech ◽  
Maurício Veloso Brun ◽  
Antonio Sergio Varela Junior ◽  
Carine Dahl Corcini
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Defense ◽  
Abdominal Cavity ◽  
Antioxidant Defense System ◽  
System Capacity ◽  
Negative Effects ◽  
Exclusion Criteria ◽  
Tissue Ischemia ◽  
Histological Damage ◽  
Laparoscopic Surgical Procedures

Pneumoperitoneum is characterized by the presence of abdominal cavity gas. Thus, this is used as a tool to create a space in the abdominal cavity for video laparoscopic surgical procedures. However, insufflation of abdominal cavity is capable of causing damage induced by tissue ischemia and reperfusion, which is caused by hypoxia and an imbalance between free radical production and antioxidant defense system capacity. The objective of this study was to bibliographic review the negative effects of exposing healthy animals to different pneumoperitoneum settings by assessing oxidative stress and testicular histopathology, identifying intra-abdominal pressures that did not result in testicular alteration. A systematic search was carried out in three databases using the following terms: pneumoperitoneum AND testi* or gonad. The survey conducted in the databases yielded 2209 scientific articles. After applying inclusion and exclusion criteria, six papers were selected. All the articles selected addressed the effects of pneumoperitoneum on testicular structure and used at least one scoring system to perform histopathological evaluation of the testis. Three studies verified the occurrence of changes in oxidative stress. According to this literature review, pneumoperitoneum used at intra-abdominal pressures equal to, or greater than, 9 mmHg caused testicular histological damage. According to the biomarkers used in studies, pressures greater than 10 mmHg were sufficient to cause testicular oxidative stress.

Differences in susceptibility to develop parameters of diabetic nephropathy in four mouse strains with type 1 diabetes

2014 ◽  
Vol 306 (10) ◽  
pp. F1171-F1178 ◽  
Author(s):  
Stephanie Franzén ◽  
Malou Friederich-Persson ◽  
Angelica Fasching ◽  
Peter Hansell ◽  
Masaomi Nangaku ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 1 Diabetes ◽  
Diabetic Nephropathy ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Mouse Strains ◽  
Histological Damage ◽  
Glomerular Damage

One-third of diabetes mellitus patients develop diabetic nephropathy, and with underlying mechanisms unknown it is imperative that diabetic animal models resemble human disease. The present study investigated the susceptibility to develop diabetic nephropathy in four commonly used and commercially available mouse strains with type 1 diabetes to determine the suitability of each strain. Type 1 diabetes was induced in C57Bl/6, NMRI, BALB/c, and 129Sv mice by alloxan, and conscious glomerular filtration rate, proteinuria, and oxidative stress levels were measured in control and diabetic animals at baseline and after 5 and 10 wk. Histological alterations were analyzed using periodic acid-Schiff staining. Diabetic C57Bl/6 displayed increased glomerular filtration rate, i.e., hyperfiltration, whereas all other parameters remained unchanged. Diabetic NMRI developed the most pronounced hyperfiltration as well as increased oxidative stress and proteinuria but without glomerular damage. Diabetic BALB/c did not develop hyperfiltration but presented with pronounced proteinuria, increased oxidative stress, and glomerular damage. Diabetic 129Sv displayed proteinuria and increased oxidative stress without glomerular hyperfiltration or damage. However, all strains displayed intrastrain correlation between oxidative stress and proteinuria. In conclusion, diabetic C57Bl/6 and NMRI both developed glomerular hyperfiltration but neither presented with histological damage, although NMRI developed low-degree proteinuria. Thus these strains may be suitable when investigating the mechanism causing hyperfiltration. Neither BALB/c nor 129Sv developed hyperfiltration although both developed pronounced proteinuria. However, only BALB/c developed detectable histological damage. Thus BALB/c may be suitable when studying the roles of proteinuria and histological alterations for the progression of diabetic nephropathy.

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