α-Tocopherol depletion eliminates the regional differences in adrenal mitochondrial lipid peroxidation

1989 ◽  
Vol 62 (2) ◽  
pp. 189-195 ◽  
Author(s):  
D.A. Staats ◽  
auj]D.P. Lohr ◽  
H.D. Colby
Author(s):  
Sainath R. Kotha ◽  
Travis O. Gurney ◽  
Miles U. Magalang ◽  
Thomas J. Hund ◽  
Abhay R. Satoskar ◽  
...  

1997 ◽  
Vol 29 (Sup 1) ◽  
pp. S63-S72 ◽  
Author(s):  
Palmira Bernocchi ◽  
Claudio Ceconi ◽  
Anna Cargnoni ◽  
Paolo Pedersini ◽  
Antonella Boraso ◽  
...  

Planta Medica ◽  
2000 ◽  
Vol 66 (6) ◽  
pp. 569-571 ◽  
Author(s):  
Hiroyuki Haraguchi ◽  
Junji Inoue ◽  
Yukiyoshi Tamura ◽  
Kenji Mizutani

Brain ◽  
2015 ◽  
Vol 138 (7) ◽  
pp. 1801-1816 ◽  
Author(s):  
Kerri J. Kinghorn ◽  
Jorge Iván Castillo-Quan ◽  
Fernando Bartolome ◽  
Plamena R. Angelova ◽  
Li Li ◽  
...  

2021 ◽  
Author(s):  
Yeshvandra Verma ◽  
Kavita Rana ◽  
Varsha Rani ◽  
Suresh VS Rana

Abstract Present study reports on the hepatotoxic manifestations of arsenic trioxide loaded poly lactide-co-glycolide nanoparticles (As2O3-PLGA- NPs) in rats. As2O3-PLGA- NPs enhances the activity of serum transaminases. As2O3-PLGA-NPs are potential inducer of lipid peroxidation in mitochondria as well as microsomes. Mitochondrial lipid peroxidation was higher than the microsomal lipid peroxidation. CYP450 2E1 was lower in the liver of As2O3-PLGA- NPs treated rats in comparison to arsenic trioxide treated rats. GSH showed lower values than control rats and arsenic trioxide treated rats. Glutathione-S-transferase inhibited by arsenic trioxide, non significant increase was recorded in the liver of As2O3-PLGA- NPs treated rats. As2O3-PLGA- NPs readily accumulates in liver and induces peculiar histopathological changes viz. intracytoplasmic/intranuclear inclusions and apoptosis. Since As2O3-PLGA- NPs are being considered as a suitable chemo-preventive agent against different types of cancer, its toxicological properties are of prime concern from bio-safety point of view. Thus, present observations seem to be important from human health risk assessment point of view.


2021 ◽  
Author(s):  
Yeshvandra Verma ◽  
Kavita Rana ◽  
Varsha Rani ◽  
S VS Rana

Abstract Present study reports on the hepatotoxic manifestations of arsenic trioxide loaded poly lactide-co-glycolide nanoparticles (As2O3-PLGA- NPs) in rats. As2O3-PLGA- NPs enhances the activity of serum transaminases. As2O3-PLGA-NPs are potential inducer of lipid peroxidation in mitochondria as well as microsomes. Mitochondrial lipid peroxidation was higher than the microsomal lipid peroxidation. CYP450 2E1 was lower in the liver of As2O3-PLGA- NPs treated rats in comparison to arsenic trioxide treated rats. GSH showed lower values than control rats and arsenic trioxide treated rats. Glutathione-S-transferase inhibited by arsenic trioxide, non significant increase was recorded in the liver of As2O3-PLGA- NPs treated rats. As2O3-PLGA- NPs readily accumulates in liver and induces peculiar histopathological changes viz. intracytoplasmic/intranuclear inclusions and apoptosis. Since As2O3-PLGA- NPs are being considered as a suitable chemo-preventive agent against different types of cancer, its toxicological properties are of prime concern from bio-safety point of view. Thus, present observations seem to be important from human health risk assessment point of view.


2013 ◽  
Vol 23 ◽  
pp. S359-S360
Author(s):  
L. Jornada ◽  
A. Steckert ◽  
F. Scussel ◽  
G. Ferreira ◽  
E. Streck ◽  
...  

2010 ◽  
Vol 61 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Seema Sharma ◽  
Suresh Rana

Melatonin Inhibits Benzene-Induced Lipid Peroxidation in Rat LiverWe studied the antioxidative role of melatonin against benzene toxicity in rat liver. The inhibition of mitochondrial and microsomal lipid peroxidation differed between 24-hour (single-dose), 15-day, and 30-day treatments. Inhibition of mitochondrial lipid peroxidation was the highest after the single dose of melatonin, whereas highest microsomal inhibition was recorded after 30 days of melatonin treatment. No significant difference was recorded between 15-day and 30-day treatments. Cytochrome P 4502E1 (CYP 4502E1) activity declined after the single-dose and 15-day melatonin treatment in the benzene-treated group, but it rose again, though not significantly after 30 days of treatment. Liver histopathology generally supported these findings. Phenol concentration in the urine samples declined in melatonin and benzene-treated rats. Our results show that melatonin affects CYP 4502E1, which is responsible for benzene metabolism. Inhibition of its metabolism correlated with lower lipid peroxidation. In conclusion, melatonin was found to be protective against lipid peroxidation induced by benzene.


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