scholarly journals Calmangafodipir Reduces Sensory Alterations and Prevents Intraepidermal Nerve Fibers Loss in a Mouse Model of Oxaliplatin Induced Peripheral Neurotoxicity

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 594 ◽  
Author(s):  
Annalisa Canta ◽  
Alessia Chiorazzi ◽  
Eleonora Pozzi ◽  
Giulia Fumagalli ◽  
Laura Monza ◽  
...  
Keyword(s):  
Mouse Model ◽  
Thermal Hyperalgesia ◽  
Nerve Fibers ◽  
Peripheral Neurotoxicity ◽  
Mitochondrial Superoxide ◽  
Key Factor ◽  
Skin Biopsies ◽  
Pre Treatment ◽  
Mitochondrial Superoxide Dismutase ◽  
Intraepidermal Nerve Fiber

Oxaliplatin (OHP) is an antineoplastic compound able to induce peripheral neurotoxicity. Oxidative stress has been suggested to be a key factor in the development of OHP-related peripheral neurotoxicity. Mangafodipir, a contrast agent possessing mitochondrial superoxide dismutase (MnSOD)-mimetic activity, has been tested as a cytoprotector in chemotherapy-induced peripheral neurotoxicity (CIPN). Calmangafodipir (PledOx®) has even better therapeutic activity. We investigated a BALB/c mouse model of OHP-related CIPN and the effects of the pre-treatment of calmangafodipir (2.5, 5, or 10 mg/kg intravenously) on sensory perception, and we performed a pathological study on skin biopsies to assess intraepidermal nerve fiber (IENF) density. At the end of the treatments, OHP alone or in pre-treatment with calmangafodipir 2.5 and 10 mg/kg, induced mechanical allodynia and cold thermal hyperalgesia, but calmangafodipir 5 mg/kg prevented these effects. Accordingly, OHP alone or in pre-treatment with calmangafodipir 2.5 and 10 mg/kg, induced a significant reduction in IENF density, but calmangafodipir 5 mg/kg prevented this reduction. These results confirm a protective effect of calmangafodipir against OHP-induced small fiber neuropathy. Interestingly, these results are in agreement with previous observations suggesting a U-shaped effect of calmangafodipir, with the 10 mg/kg dose less effective than the lower doses.

scholarly journals Reply to a Comment Paper on the Published Paper by Canta, A. et al: “Calmangafodipir Reduces Sensory Alterations and Prevents Intraepidermal Nerve Fibers Loss in a Mouse Model of Oxaliplatin Induced Peripheral Neurotoxicity”—Antioxidants 2020, 9, 594

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 807
Author(s):  
Annalisa Canta ◽  
Alessia Chiorazzi ◽  
Eleonora Pozzi ◽  
Giulia Fumagalli ◽  
Laura Monza ◽  
...  
Keyword(s):  
Mouse Model ◽  
Nerve Fiber ◽  
Protective Action ◽  
Mechanisms Of Action ◽  
Nerve Fibers ◽  
Peripheral Neurotoxicity ◽  
Published Paper ◽  
Intraepidermal Nerve Fiber

The comments sent by Stehr, Lundstom and Karlsson with reference to our article “Calmangafodipir reduces sensory alterations and prevents intraepidermal nerve fiber loss in a mouse model of oxaliplatin-induced peripheral neurotoxicity“ are very interesting, since they suggest possible mechanisms of action of the compound, which might contribute to its protective action [...]

scholarly journals Comment on “Calmangafodipir Reduces Sensory Alterations and Prevents Intraepidermal Nerve Fibers Loss in a Mouse Model of Oxaliplatin Induced Peripheral Neurotoxicity” Antioxidants 2020, 9, 594

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 802
Author(s):  
Jan Eric Stehr ◽  
Ingemar Lundström ◽  
Jan Olof G. Karlsson
Keyword(s):  
Mouse Model ◽  
Nerve Fibers ◽  
Peripheral Neurotoxicity

We have with enthusiasm read the article “Calmangafodipir Reduces Sensory Alterations and Prevents Intraepidermal Nerve Fibers Loss in a Mouse Model of Oxaliplatin Induced Peripheral Neurotoxicity” written by Annalisa Canta, Guido Cavaletti and co-workers and published in Antioxidants [...]

Diazoxide Modulates Cardiac Hypertrophy by Targeting H2O2 Generation and Mitochondrial Superoxide Dismutase Activity

2020 ◽  
Vol 13 (1) ◽  
pp. 76-83
Author(s):  
Aline Maria Brito Lucas ◽  
Joana Varlla de Lacerda Alexandre ◽  
Maria Thalyne Silva Araújo ◽  
Cicera Edna Barbosa David ◽  
Yuana Ivia Ponte Viana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Cardiac Hypertrophy ◽  
Superoxide Dismutase Activity ◽  
Heart Weight ◽  
Pharmacological Intervention ◽  
Wall Thickening ◽  
H2o2 Production ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Superoxide Dismutase

Background: Cardiac hypertrophy involves marked wall thickening or chamber enlargement. If sustained, this condition will lead to dysfunctional mitochondria and oxidative stress. Mitochondria have ATP-sensitive K+ channels (mitoKATP) in the inner membrane that modulate the redox status of the cell. Objective: We investigated the in vivo effects of mitoKATP opening on oxidative stress in isoproterenol- induced cardiac hypertrophy. Methods: Cardiac hypertrophy was induced in Swiss mice treated intraperitoneally with isoproterenol (ISO - 30 mg/kg/day) for 8 days. From day 4, diazoxide (DZX - 5 mg/kg/day) was used in order to open mitoKATP (a clinically relevant therapy scheme) and 5-hydroxydecanoate (5HD - 5 mg/kg/day) or glibenclamide (GLI - 3 mg/kg/day) were used as mitoKATP blockers. Results: Isoproterenol-treated mice had elevated heart weight/tibia length ratios (HW/TL). Additionally, hypertrophic hearts had elevated levels of carbonylated proteins and Thiobarbituric Acid Reactive Substances (TBARS), markers of protein and lipid oxidation. In contrast, mitoKATP opening with DZX avoided ISO effects on gross hypertrophic markers (HW/TL), carbonylated proteins and TBARS, in a manner reversed by 5HD and GLI. Moreover, DZX improved mitochondrial superoxide dismutase activity. This effect was also blocked by 5HD and GLI. Additionally, ex vivo treatment of isoproterenol- induced hypertrophic cardiac tissue with DZX decreased H2O2 production in a manner sensitive to 5HD, indicating that this drug also acutely avoids oxidative stress. Conclusion: Our results suggest that diazoxide blocks oxidative stress and reverses cardiac hypertrophy. This pharmacological intervention could be a potential therapeutic strategy to prevent oxidative stress associated with cardiac hypertrophy.

SOD2 Functions Downstream of Sch9 to Extend Longevity in Yeast

Genetics ◽  
2003 ◽  
Vol 163 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Paola Fabrizio ◽  
Lee-Loung Liou ◽  
Vanessa N Moy ◽  
Alberto Diaspro ◽  
Joan Selverstone Valentine ◽  
...  
Keyword(s):  
Life Span ◽  
Stress Resistance ◽  
Reversible Inactivation ◽  
Life Span Extension ◽  
Resistance Proteins ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Aconitase ◽  
Chronological Life Span ◽  
Survival Extension ◽  
Mitochondrial Superoxide Dismutase

Abstract Signal transduction pathways inactivated during periods of starvation are implicated in the regulation of longevity in organisms ranging from yeast to mammals, but the mechanisms responsible for life-span extension are poorly understood. Chronological life-span extension in S. cerevisiae cyr1 and sch9 mutants is mediated by the stress-resistance proteins Msn2/Msn4 and Rim15. Here we show that mitochondrial superoxide dismutase (Sod2) is required for survival extension in yeast. Deletion of SOD2 abolishes life-span extension in sch9Δ mutants and decreases survival in cyr1:mTn mutants. The overexpression of Sods—mitochondrial Sod2 and cytosolic CuZnSod (Sod1)—delays the age-dependent reversible inactivation of mitochondrial aconitase, a superoxide-sensitive enzyme, and extends survival by 30%. Deletion of the RAS2 gene, which functions upstream of CYR1, also doubles the mean life span by a mechanism that requires Msn2/4 and Sod2. These findings link mutations that extend chronological life span in S. cerevisiae to superoxide dismutases and suggest that the induction of other stress-resistance genes regulated by Msn2/4 and Rim15 is required for maximum longevity extension.

scholarly journals NEUROPROTECTION OF ABELMOSCHUS ESCULENTUS L. AGAINST DIABETIC NEUROPATHY

2018 ◽  
Vol 11 (15) ◽  
pp. 28
Author(s):  
Lee Wei Yang ◽  
Santosh Fattepur ◽  
Kiran Chanabasappa Nilugal ◽  
Fadli Asmani ◽  
Eddy Yusuf ◽  
...  
Keyword(s):  
Body Weight ◽  
Sciatic Nerve ◽  
Diabetic Neuropathy ◽  
Performance Test ◽  
Neuroprotective Effect ◽  
Thermal Hyperalgesia ◽  
Diabetic Rats ◽  
Nerve Fibers ◽  
Abelmoschus Esculentus ◽  
Rotarod Performance

Objective: The present study was designed to determine the neuroprotective effect of Abelmoschus esculentus L. on alloxan-induced diabetic neuropathy in rats.Methods: Diabetes was induced in rats with a single intraperitoneal injection of alloxan monohydrate (130 mg/kg b.w). The ethanol extract of A. esculentus L. at a dose of 100 and 200 mg/kg of body weight was administered at single dose per day to alloxan-induced diabetic rats for 21 days. The fasting blood glucose was screened in the intermittent on day 0, day 14, and day 21. Behavioral tests such as thermal hyperalgesia test and rotarod performance test were performed to assess the thermal sensitivity and muscle grip strength. At the end of the study period, experimental animals were sacrificed and sciatic nerve tissues were obtained for histopathological investigation.Results: Animals treated with A. esculentus L. extarct at a dose of 200 mg/kg of body weight significantly reduced (p<0.05) in hyperglycemia and thermal hyperalgesia and significantly increased (p<0.05) in rotarod performance. The sciatic nerve fiber of diabetic rats receiving 200 mg/kg of body weight of A. esculentus L. extract also shows no swelling of nerve fibers, and lesser demyelination was observed.Conclusion: These findings demonstrate that A. esculentus L. exhibits significant antidiabetic and neuroprotective effect against alloxan-induced diabetic neuropathy in rats.

Immunoreactivity and activity of mitochondrial superoxide dismutase following training and exercise

1994 ◽  
Vol 1 (3) ◽  
pp. 165-168 ◽  
Author(s):  
Chandan K. Sen ◽  
Tomomi Ookawara ◽  
Keiichiro Suzuki ◽  
Naoyuki Taniguchi ◽  
Osmo Hänninen ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Superoxide Dismutase
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