Effects of in Vivo Captan Administration on Cytotoxicity, Gluconeogenesis, ATP Levels, and Parameters Related to Oxidative Stress in Rat Liver

1999 ◽  
Vol 64 (3) ◽  
pp. 185-193 ◽  
Author(s):  
M.J. Moreno-Aliaga ◽  
J.C. Arenas-Vidal ◽  
A. Berjóaan ◽  
M.P. Fernández-Otero
1993 ◽  
Vol 194 (2) ◽  
pp. 635-641 ◽  
Author(s):  
M.A. Pronzato ◽  
C. Domenicotti ◽  
E. Rosso ◽  
A. Bellocchio ◽  
M. Patrone ◽  
...  

2021 ◽  
Vol 22 (20) ◽  
pp. 11219
Author(s):  
Nadia Z. Shaban ◽  
Salah A. Yehia ◽  
Doaa Awad ◽  
Shaban Y. Shaban ◽  
Samar R. Saleh

Titanium (IV)–dithiophenolate complex chitosan nanocomposites (DBT–CSNPs) are featured by their antibacterial activities, cytotoxicity, and capacity to bind with DNA helixes. In this study, their therapeutic effects against rat liver damage induced by carbon tetrachloride (CCl4) and their anti-proliferative activity against human liver cancer (HepG2) cell lines were determined. Results of treatment were compared with cisplatin treatment. Markers of apoptosis, oxidative stress, liver functions, and liver histopathology were determined. The results showed that DBT–CSNPs and DBT treatments abolished liver damage induced by CCl4 and improved liver architecture and functions. DNA fragmentation, Bax, and caspase-8 were reduced, but Bcl-2 and the Bcl-2/Bax ratios were increased. However, there was a non-significant change in the oxidative stress markers. DBT–CSNPs and DBT inhibited the proliferation of HepG2 cells by arresting cells in the G2/M phase and inducing cell death. DBT–CSNPs were more efficient than DBT. Low doses of DBT and DBT–CSNPs applied to healthy rats for 14 days had no adverse effect. DBT and DBT–CSNP treatment gave preferable results than the treatment with cisplatin. In conclusion, DBT–CSNPs and DBT have anti-apoptotic activities against liver injuries and have anti-neoplastic impacts. DBT–CSNPs are more efficient. Both compounds can be used in pharmacological fields.


2003 ◽  
Vol 51 (20) ◽  
pp. 6073-6079 ◽  
Author(s):  
Kiyomi Kikugawa ◽  
Yoshinobu Yasuhara ◽  
Ken Ando ◽  
Keiko Koyama ◽  
Kazuyuki Hiramoto ◽  
...  

2017 ◽  
Vol 36 (1) ◽  
pp. 4-12 ◽  
Author(s):  
Marcos Rodrigues Maldonado ◽  
Lívia Bracht ◽  
Anacharis Babeto de Sá-Nakanishi ◽  
Rúbia Carvalho Gomes Corrêa ◽  
Jurandir Fernando Comar ◽  
...  

Biochimie ◽  
2020 ◽  
Vol 171-172 ◽  
pp. 187-196
Author(s):  
Nevton Teixeira da Rosa-Junior ◽  
Belisa Parmeggiani ◽  
Nícolas Manzke Glänzel ◽  
Leonardo de Moura Alvorcem ◽  
Marina Rocha Frusciante ◽  
...  

Author(s):  
Simon Couly ◽  
Bilal Khalil ◽  
Véronique Viguier ◽  
Julien Roussel ◽  
Tangui Maurice ◽  
...  

Abstract Sigma-1 receptor (S1R) is an endoplasmic reticulum (ER) chaperone that regulates mitochondrial respiration but also controls cellular defense against ER and oxidative stress. This makes S1R a potential therapeutic target in amyotrophic lateral sclerosis (ALS). Especially, as a missense mutation E102Q in S1R has been reported in few familial ALS cases. However, the pathogenicity of S1RE102Q and the beneficial impact of S1R in the ALS context remain to be demonstrated in vivo. To address this, we generated transgenic Drosophila that express human wild-type S1R or S1RE102Q. Expression of mutant S1R in fly neurons induces abnormal eye morphology and locomotor defects in a dose-dependent manner. This was accompanied by abnormal mitochondrial fragmentation, reduced ATP levels and a higher fatigability at the neuromuscular junction during high energy demand. Overexpressing IP3 receptor or glucose transporter mitigates the S1RE102Q-induced eye phenotype, further highlighting the role of calcium and energy metabolism in its toxicity. More importantly, we showed that wild-type S1R rescues locomotor activity and ATP levels of flies expressing the key ALS protein, TDP43. Moreover, overexpressing wild-type S1R enhances resistance of flies to oxidative stress. Therefore, our data provide the first genetic evidence that mutant S1R recapitulates ALS pathology in vivo while increasing S1R confers neuroprotection against TDP43 toxicity.


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