The prospective protective effect of selenium nanoparticles against chromium-induced oxidative and cellular damage in rat thyroid

Erythropoietic protoporphyria (EPP) is a disease associated with ferrochelatase deficiency and characterized by the accumulation of protoporphyrin IX (PROTO IX) in erythrocytes, liver, and skin. In some cases, a severe hepatic failure and cholestasis were observed. Griseofulvin (Gris) develops an experimental EPP with hepatic manifestations in mice such as PROTO IX accumulation followed by cellular damage as wells as necrotic and inflammatory processes. The antioxidant defense system was also altered. The aim was to evaluate the possible protective effect of different antioxidant compounds: trolox (Tx), ascorbic acid (Asc), the combination Tx and Asc, melatonin (Mel), and the polyphenols: ellagic acid, quercetin, chlorogenic acid, caffeic acid, gallic acid, and ferulic acid on liver damage and oxidative stress markers in a mouse model of EPP. Coadministration of Gris with Tx, Asc, and its combination, or Mel mainly affected heme biosynthetic pathway, resulting in a decrease in ALA-S activity which was increased by Gris, while the tested polyphenols exerted a protective effect on oxidative stress, decreasing lipid peroxidation and the activity of some antioxidant enzymes. In conclusion, antioxidant compounds can only protect partially against the liver damage induced by Gris, reducing oxidative stress or acting on heme regulation.

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Protective effect of coenzyme Q10 against hypoxic cellular damage.

Chemical and Pharmaceutical Bulletin ◽

10.1248/cpb.33.2896 ◽

1985 ◽

Vol 33 (7) ◽

pp. 2896-2903 ◽

Cited By ~ 4

Author(s):

NOBORU SUZUKI ◽

TETSUYA NAKAMURA ◽

HIDEYUKI ISHIDA ◽

KIYOSHI HOSONO

Keyword(s):

Protective Effect ◽

Coenzyme Q10 ◽

Cellular Damage

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Protective Effect and Mechanism of Total Flavones fromRhododendron simsiiPlanch Flower on Cultured Rat Cardiomyocytes with Anoxia and Reoxygenation

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2015/863531 ◽

2015 ◽

Vol 2015 ◽

pp. 1-10 ◽

Cited By ~ 6

Author(s):

Yi Jiao ◽

Yi-Fei Fan ◽

Yu-Ling Wang ◽

Jun-Yan Zhang ◽

Shuo Chen ◽

...

Keyword(s):

Myocardial Infarction ◽

Protective Effect ◽

Cell Viability ◽

Ischemia Reperfusion ◽

Cellular Damage ◽

Protective Mechanism ◽

Patch Clamp Technique ◽

Rat Cardiomyocytes ◽

Whole Cell Patch Clamp ◽

Myocardial Ischemia Reperfusion

Many flavonoids have cardioprotection against myocardial ischemia/reperfusion (I/R) injury. Total flavones fromRhododendron simsiiPlanch flower (TFR) can protect myocardial ischemic injuries. However, its protective mechanism is still unknown. The present study was designed to investigate the mechanism of TFR on myocardial I/R and anoxia/reoxygenation (A/R) injuries. Rat model of myocardial I/R injury was made, and myocardial infarction was determined. A/R injury was induced in cultured rat cardiomyocytes; cellular damage was evaluated by measuring cell viability, LDH and cTnT releases, and MDA content. Expressions of ROCK1and ROCK2protein were examined by Western blot analysis, and K+currents were recorded by using whole-cell patch clamp technique. TFR 20~80 mg/kg markedly reduced I/R-induced myocardial infarction. TFR 3.7~300 mg/L significantly inhibited A/R-induced reduction of cell viability, LDH and cTnT releases, and MDA production. Exposure to A/R significantly increased ROCK1and ROCK2expressions in rat cardiomyocytes, but TFR 33.3~300 mg/L obviously inhibited this increase. 300 mg/L TFR significantly augmented inward rectifier K+current and other K+currents in rat cardiomyocytes. These results indicate that TFR has a protective effect on rat cardiomyocytes A/R damage, and the protective mechanism may be engaged with the inhibition of ROCK1and ROCK2and activation of K+channels.

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Protective effect of starch-stabilized selenium nanoparticles against melamine-induced hepato-renal toxicity in male albino rats

International Journal of Biological Macromolecules ◽

10.1016/j.ijbiomac.2021.09.156 ◽

2021 ◽

Author(s):

Zainab Sabry Othman Ahmed ◽

Mona K. Galal ◽

Elsayed A. Drweesh ◽

Khaled S. Abou-El-Sherbini ◽

Eman A.M. Elzahany ◽

...

Keyword(s):

Protective Effect ◽

Renal Toxicity ◽

Selenium Nanoparticles ◽

Albino Rats

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The protective effect of selenium from heat stress-induced porcine small intestinal epithelial cell line (IPEC-J2) injury is associated with regulation expression of selenoproteins

British Journal Of Nutrition ◽

10.1017/s0007114519001910 ◽

2019 ◽

Vol 122 (10) ◽

pp. 1081-1090

Author(s):

Jiayong Tang ◽

Lei Cao ◽

Gang Jia ◽

Guangmang Liu ◽

Xiaoling Chen ◽

...

Keyword(s):

Heat Stress ◽

Protective Effect ◽

Cell Viability ◽

Cell Injury ◽

Negative Impact ◽

Cellular Damage ◽

Epithelial Cell Line ◽

Glutathione Peroxidase 1 ◽

Protein Levels ◽

Encoding Genes

AbstractThe present study compared the protective effect of sodium selenite (SS) and selenomethionine (SeMet) on heat stress (HS)-invoked porcine IPEC-J2 cellular damage and integrate potential roles of corresponding selenoprotein. Cells were cultured at 37°C until 80 % confluence and then subjected to four different conditions for 24 h: at 37°C (control), 41·5°C (HS), 41·5°C supplied with 0·42 µmol Se/L SS (SS), or SeMet (SeMet). HS significantly decreased cell viability, up-regulated mRNA and protein levels of heat shock protein 70 (HSP70) and down-regulated mRNA and protein levels of tight junction-related proteins (claudin-1 (CLDN-1) and zonula occludens-1 (ZO-1)). HS-induced cell injury was associated with the up-regulation (P < 0·05) of six inflammation-related genes and fourteen selenoprotein encoding genes and down-regulation (P < 0·05) of two inflammation-related genes and five selenoprotein encoding genes. Compared with the HS group, SS and SeMet supplementation resulted in an increase (P < 0·05) in cell viability, decreased (P < 0·05) mRNA expression of HSP70 and six inflammation-related genes and rescue (P < 0·05) of mRNA and protein levels of CLDN-1 and ZO-1. SS and SeMet supplementation changes the expressions of nineteen selenoprotein encoding genes in cells affected by HS. Both Se supplementation significantly recovered the protein level of glutathione peroxidase-1 and increased selenoprotein P in the IPEC-J2 cells under HS, respectively. In summary, Se supplementation alleviated the negative impact of HS on IPEC-J2 cells, and their cellular protective effect was associated with regulation expression of selenoproteins, and SeMet exhibited a better protective effect.

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Nitroxide Radical-Containing Redox Nanoparticles Protect Neuroblastoma SH-SY5Y Cells against 6-Hydroxydopamine Toxicity

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/9260748 ◽

2020 ◽

Vol 2020 ◽

pp. 1-19 ◽

Cited By ~ 1

Author(s):

Monika Pichla ◽

Łukasz Pulaski ◽

Katarzyna Dominika Kania ◽

Ireneusz Stefaniuk ◽

Bogumił Cieniek ◽

...

Keyword(s):

Protective Effect ◽

Antioxidant Properties ◽

Cellular Damage ◽

Cellular Model ◽

Mitochondrial Potential ◽

Human Neuroblastoma ◽

Mitochondrial Mass ◽

Mitochondrial Superoxide ◽

6 Hydroxydopamine

Parkinson’s disease (PD) patients can benefit from antioxidant supplementation, and new efficient antioxidants are needed. The aim of this study was to evaluate the protective effect of selected nitroxide-containing redox nanoparticles (NRNPs) in a cellular model of PD. Antioxidant properties of NRNPs were studied in cell-free systems by protection of dihydrorhodamine 123 against oxidation by 3-morpholino-sydnonimine and protection of fluorescein against bleaching by 2,2-azobis(2-amidinopropane) hydrochloride and sodium hypochlorite. Model blood-brain barrier penetration was studied using hCMEC/D3 cells. Human neuroblastoma SH-SY5Y cells, exposed to 6-hydroxydopamine (6-OHDA), were used as an in vitro model of PD. Cells were preexposed to NRNPs or free nitroxides (TEMPO or 4-amino-TEMPO) for 2 h and treated with 6-OHDA for 1 h and 24 h. The reactive oxygen species (ROS) level was estimated with dihydroethidine 123 and Fluorimetric Mitochondrial Superoxide Activity Assay Kit. Glutathione level (GSH) was measured with ortho-phtalaldehyde, ATP by luminometry, changes in mitochondrial membrane potential with JC-1, and mitochondrial mass with 10-Nonyl-Acridine Orange. NRNP1, TEMPO, and 4-amino-TEMPO (25-150 μM) protected SH-SY5Y cells from 6-OHDA-induced viability loss; the protection was much higher for NRNP1 than for free nitroxides. NRNP1 were better antioxidants in vitro and permeated better the model BBB than free nitroxides. Exposure to 6-OHDA decreased the GSH level after 1 h and increased it considerably after 24 h (apparently a compensatory overresponse); NRNPs and free nitroxides prevented this increase. NRNP1 and free nitroxides prevented the decrease in ATP level after 1 h and increased it after 24 h. 6-OHDA increased the intracellular ROS level and mitochondrial superoxide level. Studied antioxidants mostly decreased ROS and superoxide levels. 6-OHDA decreased the mitochondrial potential and mitochondrial mass; both effects were prevented by NRNP1 and nitroxides. These results suggest that the mitochondria are the main site of 6-OHDA-induced cellular damage and demonstrate a protective effect of NRNP1 in a cellular model of PD.

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