JM-20, a novel hybrid molecule, protects against rotenone-induced neurotoxicity in experimental model of Parkinson’s disease

Fonseca-Fonseca, Luis Arturo; Wong-Guerra, Maylin; Ramírez-Sánchez, Jeney; Montano-Peguero, Yanay; Yaquis, Alejandro Saúl Padrón; Rodríguez, Abel Mondelo; Silva, Víctor Diógenes Amaral da; Costa, Sílvia Lima; Pardo-Andreu, Gilberto L.; Nuñez-Figueredo, Yanier

doi:10.1016/j.neulet.2018.10.008

Cited by 15 publications

(12 citation statements)

References 21 publications

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“…Fonseca-Fonseca LA and co-authors support this mechanism. They found that mitochondria isolated from brain of rats with PD, induced by ROT, spontaneously lost their membrane potential and were more prone to membrane permeability/swelling than the vehicle group [10]. Here we observed a decrease in the intensity of LTR in rats following ROT administration.…”

Section: Discussionsupporting

confidence: 52%

“…In this context, the drugs with the ability to modulate mitochondrial dynamics, function and biogenesis may have important clinical applications in the future treatment of PD. L.A. Fonseca et al showed that benzodiazepine-derivative substances protect the neuronal mitochondria against ROT-induced damage in rats model of PD [10]. Ukrainian scientists have developed the chemical compounds of the class of 2.3-benzodiazepines, which are characterized by the activity in relation to CNS.…”

Section: Introductionmentioning

confidence: 99%

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The evaluation of 2.3-diazepine influence on tissue respiration of the liver and its exocrine function in rats with a rotenone model of Parkinson’s disease

et al. 2019

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Parkinson's disease (PD) is a progressive neurodegenerative disorder, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. The causes of PD are not fully understood; however, increasing evidence implicates disturbed respiratory function of the mitochondria and a lack of energy in cells. Aim. To study the effects of 2.3-diazepine (2.3-DP), a new derivative of benzodiazepine, on liver tissue respiration (LTR) and energy dependent processes of bile and bile acids (BAs) production in a rat model of PD. Methods. PD was induced by intraperitoneal injections of rotenone (ROT). LTR (the intensity of the oxygen uptake) was assessed using the polarograph LP-9 (Czech Republic). Secreted bile was collected during 1 hour of the experiment through the polyethylene catheter inserted into the common bile duct. BAs were separated by the method of thin layer chromatography. Results. ROT diminished the index of liver oxygen consumption by 34 % (p<0.001), reduced bile flow by 33.8 % (p<0.001) and disturbed the conjugation of cholic acid with amino acids taurine and glycine reducing the index of conjugation by 29.2 % (p<0.001). ROT also increased by 25.6 % (p<0.001) the part of acidic pathway in the biosynthesis of BAs. The application of 2.3-DP results in full or partial recovery of LTR, bile flow, concentrations of BAs and their ratio in the bile of rats with PD. Conclusion. 2.3-DP markedly affected function of the liver parenchyma in a rat model of PD. This drug changed the intensity of LTR, bile flow and notably modified bile chemical compositions.

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Section: Discussionsupporting

confidence: 52%

Section: Introductionmentioning

confidence: 99%

The evaluation of 2.3-diazepine influence on tissue respiration of the liver and its exocrine function in rats with a rotenone model of Parkinson’s disease

et al. 2019

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“…In this context, the drugs with the ability to modulate mitochondrial function and biogenesis may have important clinical significance in the future treatment of PD. In recent years, the data of science literature have demonstrated in rats model of PD that in neurodegenerative disorders, such as PD, antipsychotic drugs, in particular benzodiazepine derivatives, protect the neuronal mitochondria against ROT-induced damage [13]. Benzodiazepines reduce skeletal muscle tone (effect associated with suppression of polysynaptic reflexes at spinal cord level) and demonstrate anticonvulsant activity, potentiate the action of substances that suppress the central nervous system [14].…”

mentioning

confidence: 99%

Diazepinone effect on liver tissue respiration and serum lipid content in rats with a rotenone model of Parkinson’s disease

Shtanova¹,

Yanchuk²,

Veselsky³

2020

Ukr.Biochem.J

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“…The observed in the present study response of antioxidant enzymes to ROT was diversified, similarly as in other reports. In the vast majority of publications concerning the effect of ROT on antioxidant enzymes, their activities have been reduced [34][35][36][37][38][39][40][42][43][44][47][48][49][50]. However, several reports can be found in the available literature where ROT has evoked increased activities of several enzymes [41,45,46,51] or caused no alterations in their activities [37,49,51,52].…”

Section: Brainmentioning

confidence: 99%

Can Cranberry Juice Protect against Rotenone-Induced Toxicity in Rats?

et al. 2021

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The high polyphenols content of cranberry accounts for its strong antioxidant activity underlying the beneficial health effects of this fruit. Rotenone (ROT) is a specific inhibitor of mitochondrial complex I in the brain which leads to the generation of oxidative stress. To date, there are few data indicating that toxicity of ROT is not limited to the brain but can also affect other tissues. We aimed to examine whether ROT-induced oxidative stress could be counteracted by cranberry juice not only in the brain but also in the liver and kidney. Wistar rats were given the combined treatment with ROT and cranberry juice (CJ) for 35 days. Parameters of antioxidant status were determined in the organs. ROT enhanced lipid peroxidation solely in the brain. The increase in the DNA damage was noticed in all organs examined and in leukocytes. The beneficial effect of CJ on these parameters appeared only in the brain. Additionally, CJ decreased the activity of serum hepatic enzymes. The effect of CJ on antioxidant enzymes was not consistent, however, in some organs, CJ reversed changes evoked by ROT. Summing up, ROT can cause oxidative damage not only in the brain but also in other organs. CJ demonstrated a protective effect against ROT-induced toxicity.

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JM-20, a novel hybrid molecule, protects against rotenone-induced neurotoxicity in experimental model of Parkinson’s disease

Cited by 15 publications

References 21 publications

The evaluation of 2.3-diazepine influence on tissue respiration of the liver and its exocrine function in rats with a rotenone model of Parkinson’s disease

The evaluation of 2.3-diazepine influence on tissue respiration of the liver and its exocrine function in rats with a rotenone model of Parkinson’s disease

Diazepinone effect on liver tissue respiration and serum lipid content in rats with a rotenone model of Parkinson’s disease

Can Cranberry Juice Protect against Rotenone-Induced Toxicity in Rats?

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