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{{Abstract
{{Abstract
|title=Kolonics A, Léner V, Kutasi B, Kutasi J (2022) Effects of ''Scenedesmus rubescens'' extract on Paraquat induced parkinsonism model in SH-SY5Y cells and mitochondrial dysfunction
|title=Kolonics A, Léner V, Kutasi B, Kutasi J (2022) Effects of ''Scenedesmus rubescens'' extract on Paraquat induced parkinsonism model in SH-SY5Y cells and mitochondrial dysfunction
|info=
|authors=Kolonics Attila, Lener V, Kutasi B, Kutasi J
|authors=Kolonics Attila, Lener V, Kutasi B, Kutasi J  
|year=2022
|year=2022
|event=[[Bioblast 2022]]
|event=[[Bioblast 2022]]
|abstract=
|abstract=Parkinson's disease (PD), a common neurodegenerative disease is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. PD is an age related neurodegenerative disorder believed to originate in part via reactive oxygen species overproduction, leading to oxidative stress and mitochondrial dysfunction [1]. Paraquat (PQ<sup>2+</sup>), a widely used herbicide, is an oxidative stress inducer that has been implicated as a potential risk factor for the development of PD [2]. Scenedesmus sp., have been suggested for human nutraceutical application due to their content of the nutritious fatty acids and antioxidant pigments like astaxanthin, β-carotene, lutein and other vitamins. These pigments are naturally occurring polyphenolic compounds that display a variety of therapeutic properties in oxidative stress [3].<br>
 
Parkinson's disease (PD), a common neurodegenerative disease is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. PD is an age related neurodegenerative disorder believed to originate in part via reactive oxygen species overproduction, leading to oxidative stress and mitochondrial dysfunction [1]. Paraquat (PQ<sup>2+</sup>), a widely used herbicide, is an oxidative stress inducer that has been implicated as a potential risk factor for the development of PD [2]. Scenedesmus sp., have been suggested for human nutraceutical application due to their content of the nutritious fatty acids and antioxidant pigments like astaxanthin, β-carotene, lutein and other vitamins. These pigments are naturally occurring polyphenolic compounds that display a variety of therapeutic properties in oxidative stress [3].<br>
The effect of ''Scenedesmus rubens'' (single cell, green algae) DMSO-extract (SCO) on PQ<sup>2+</sup>-induced cellular toxicity was evaluated by measuring cell viability by MTT assay and cellular ATP production by bioluminescent luciferase assay (FLAAM) in SH-SY5Y cells after 3 days of PQ<sup>2+</sup> treatment. Direct mitochondrial effects of PQ<sup>2+</sup> vs SCO was evaluated in intact murine brain mitochondria by monitoring basal and succinate induced ROS production (Amplex Red + HRP); ΔΨm (TMRE); NADH-level by its endogenous fluorescence; complex III activity by cytC.<br>
The effect of ''Scenedesmus rubens'' (single cell, green algae) DMSO-extract (SCO) on PQ<sup>2+</sup>-induced cellular toxicity was evaluated by measuring cell viability by MTT assay and cellular ATP production by bioluminescent luciferase assay (FLAAM) in SH-SY5Y cells after 3 days of PQ<sup>2+</sup> treatment. Direct mitochondrial effects of PQ<sup>2+</sup> vs SCO was evaluated in intact murine brain mitochondria by monitoring basal and succinate induced ROS production (Amplex Red + HRP); ΔΨm (TMRE); NADH-level by its endogenous fluorescence; complex III activity by cytC.<br>
SCO treatment increased the viability of PQ<sup>2+</sup> exposed SH-SY5Y cells and elevated cellular ATP levels in State 3. PQ<sup>2+</sup> -induced elevation of basal and succinate-mediated ROS production and decrease of complex III activity was ameliorated by SCO. Succinate induced mitochondrial NADH increase was not challenged by PQ<sup>2+</sup> but it was decreased by SCO suggesting inhibition of RET.<br>
SCO treatment increased the viability of PQ<sup>2+</sup> exposed SH-SY5Y cells and elevated cellular ATP levels in State 3. PQ<sup>2+</sup> -induced elevation of basal and succinate-mediated ROS production and decrease of complex III activity was ameliorated by SCO. Succinate induced mitochondrial NADH increase was not challenged by PQ<sup>2+</sup> but it was decreased by SCO suggesting inhibition of RET.<br>


In conclusion, hydrophobic molecular species of ''Scenedesmus rubescens'' may exhibit neuroprotection against PQ<sup>2+</sup>-induced neurotoxicity and one of the potential explanantions is a bypass of mitochondrial electron flow that can be therapeutically beneficial in Parkinson's disease but also in vascular diseases affected by ischemia / reperfusion.
In conclusion, hydrophobic molecular species of ''Scenedesmus rubescens'' may exhibit neuroprotection against PQ<sup>2+</sup>-induced neurotoxicity and one of the potential explanantions is a bypass of mitochondrial electron flow that can be therapeutically beneficial in Parkinson's disease but also in vascular diseases affected by ischemia / reperfusion.
====References====
[1] Fulda S, Gorman AM, Hori O, Samali A (2010) Cellular stress responses: cell survival and cell death. Int J Cell Biol. 2010;2010:214074. doi: 10.1155/2010/214074.<br>
[2] Somayajulu-Niţu M, Sandhu JK, Cohen J, Sikorska M, Sridhar TS, Matei A, Borowy-Borowski H, Pandey S (2009) Paraquat induces oxidative stress, neuronal loss in substantia nigra region and parkinsonism in adult rats: neuroprotection and amelioration of symptoms by water-soluble formulation of coenzyme Q10. BMC Neurosci. 2009 Jul 27;10:88. doi: 10.1186/1471-2202-10-88.<br>
[3] Kent M, Welladsen HM, Mangott A, Li Y (2015) Nutritional evaluation of Australian microalgae as potential human health supplements. PLoS One. 2015 Feb 27;10(2):e0118985. doi: 10.1371/journal.pone.0118985..
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__NOTOC__
__NOTOC__
== Affiliations and author contributions ==
== Affiliations ==
Kolonics A<sup>1</sup>, Léner V<sup>2</sup>, Kutasi <sup>B3</sup>, Kutasi J<sup>3</sup><br>
::::Kolonics A<sup>1</sup>, Léner V<sup>2</sup>, Kutasi <sup>B3</sup>, Kutasi J<sup>3</sup>
 
::::#Univ of Physical Education, Budapest, Hungary
1 Univ of Physical Education, Budapest, Hungary<br>
::::#Dept of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary
::::#Albitech Biotechnological Ltd., Budapest, Hungary. [email protected]


2 Dept of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary<br>
== Figures ==
[[File:Kolonics 2022 Fig 1.png|400px|none|thumb|Figure 1:'''Effects of ''Scenedesmus rubens'' extract (SCO) on Paraquat induced cell death.''' Cells were treated with Paraquat (200 μM; 3 d) in the presence of SCO (12 μg/ml) and MTT index was measured by MTT assay in SH-SY5Y cells. Data are presented as mean ± SEM from four independent experiments *p<0.05 vs. control.]]


3 Albitech Biotechnological Ltd., Budapest, Hungary<br>
[[File:Kolonics 2022 Fig 2.png|950px|none|thumb|Figure 2:'''ROS production, NADH fluorescence in Paraquat and/or SCO treated mitochondria incubated with succinate as respiratory substrates.''' Mitochondria were isolated from Balb/c mice brain. Mitochondria was treated with 200 μM Paraquat (red line) or cotreated with 12 μg/ml SCO (purple line) and incubated in medium (30 ◦C) containing 250 mM sucrose, 0.1 mM EGTA, 20 mM Tris–HCl (pH 7.4), 2.5 mM Pi and 1 mM MgCl<sub>2</sub>. '''(A)''' Hydrogen peroxide (ROS) production was assessed by Amplex Red and horse radish peroxidase; '''(B)''' NADH concentration was followed by determining its spontaneous autofluorescence. One typical experiment is presented.]]


kolonics.attila@tf.hu
== References ==
::::#Fulda S, Gorman AM, Hori O, Samali A (2010) Cellular stress responses: cell survival and cell death. Int J Cell Biol. 2010;2010:214074. doi: 10.1155/2010/214074.
::::#Somayajulu-Niţu M, Sandhu JK, Cohen J, Sikorska M, Sridhar TS, Matei A, Borowy-Borowski H, Pandey S (2009) Paraquat induces oxidative stress, neuronal loss in substantia nigra region and parkinsonism in adult rats: neuroprotection and amelioration of symptoms by water-soluble formulation of coenzyme Q10. BMC Neurosci. 2009 Jul 27;10:88. doi: 10.1186/1471-2202-10-88.
::::#Kent M, Welladsen HM, Mangott A, Li Y (2015) Nutritional evaluation of Australian microalgae as potential human health supplements. PLoS One. 2015 Feb 27;10(2):e0118985. doi: 10.1371/journal.pone.0118985.


== Figure 1  ==
[[File:Kolonics 2022 Fig 1.png|400px|none|thumb|'''Effects of ''Scenedesmus rubens'' extract (SCO) on Paraquat induced cell death.''' Cells were treated with Paraquat (200 μM; 3 d) in the presence of SCO (12 μg/ml) and MTT index was measured by MTT assay in SH-SY5Y cells. Data are presented as mean ± SEM from four independent experiments *p<0.05 vs. control.]]
== Figure 2  ==
[[File:Kolonics 2022 Fig 2.png|950px|none|thumb|'''ROS production, NADH fluorescence in Paraquat and/or SCO treated mitochondria incubated with succinate as respiratory substrates.''' Mitochondria were isolated from Balb/c mice brain. Mitochondria was treated with 200 μM Paraquat (red line) or cotreated with 12 μg/ml SCO (purple line) and incubated in medium (30 ◦C) containing 250 mM sucrose, 0.1 mM EGTA, 20 mM Tris–HCl (pH 7.4), 2.5 mM Pi and 1 mM MgCl<sub>2</sub>. '''(A)''' Hydrogen peroxide (ROS) production was assessed by Amplex Red and horse radish peroxidase; '''(B)''' NADH concentration was followed by determining its spontaneous autofluorescence. One typical experiment is presented.]]
== Help ==
== Help ==
* [[MitoPedia: Terms and abbreviations]]
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Revision as of 13:18, 4 May 2022

Kolonics A, Léner V, Kutasi B, Kutasi J (2022) Effects of Scenedesmus rubescens extract on Paraquat induced parkinsonism model in SH-SY5Y cells and mitochondrial dysfunction

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Kolonics Attila, Lener V, Kutasi B, Kutasi J (2022)

Event: Bioblast 2022

Parkinson's disease (PD), a common neurodegenerative disease is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. PD is an age related neurodegenerative disorder believed to originate in part via reactive oxygen species overproduction, leading to oxidative stress and mitochondrial dysfunction [1]. Paraquat (PQ2+), a widely used herbicide, is an oxidative stress inducer that has been implicated as a potential risk factor for the development of PD [2]. Scenedesmus sp., have been suggested for human nutraceutical application due to their content of the nutritious fatty acids and antioxidant pigments like astaxanthin, β-carotene, lutein and other vitamins. These pigments are naturally occurring polyphenolic compounds that display a variety of therapeutic properties in oxidative stress [3].
The effect of Scenedesmus rubens (single cell, green algae) DMSO-extract (SCO) on PQ2+-induced cellular toxicity was evaluated by measuring cell viability by MTT assay and cellular ATP production by bioluminescent luciferase assay (FLAAM) in SH-SY5Y cells after 3 days of PQ2+ treatment. Direct mitochondrial effects of PQ2+ vs SCO was evaluated in intact murine brain mitochondria by monitoring basal and succinate induced ROS production (Amplex Red + HRP); ΔΨm (TMRE); NADH-level by its endogenous fluorescence; complex III activity by cytC.
SCO treatment increased the viability of PQ2+ exposed SH-SY5Y cells and elevated cellular ATP levels in State 3. PQ2+ -induced elevation of basal and succinate-mediated ROS production and decrease of complex III activity was ameliorated by SCO. Succinate induced mitochondrial NADH increase was not challenged by PQ2+ but it was decreased by SCO suggesting inhibition of RET.

In conclusion, hydrophobic molecular species of Scenedesmus rubescens may exhibit neuroprotection against PQ2+-induced neurotoxicity and one of the potential explanantions is a bypass of mitochondrial electron flow that can be therapeutically beneficial in Parkinson's disease but also in vascular diseases affected by ischemia / reperfusion.


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Affiliations

Kolonics A1, Léner V2, Kutasi B3, Kutasi J3
  1. Univ of Physical Education, Budapest, Hungary
  2. Dept of Experimental Pharmacology, National Institute of Oncology, Budapest, Hungary
  3. Albitech Biotechnological Ltd., Budapest, Hungary. [email protected]

Figures

Figure 1:Effects of Scenedesmus rubens extract (SCO) on Paraquat induced cell death. Cells were treated with Paraquat (200 μM; 3 d) in the presence of SCO (12 μg/ml) and MTT index was measured by MTT assay in SH-SY5Y cells. Data are presented as mean ± SEM from four independent experiments *p<0.05 vs. control.
Figure 2:ROS production, NADH fluorescence in Paraquat and/or SCO treated mitochondria incubated with succinate as respiratory substrates. Mitochondria were isolated from Balb/c mice brain. Mitochondria was treated with 200 μM Paraquat (red line) or cotreated with 12 μg/ml SCO (purple line) and incubated in medium (30 ◦C) containing 250 mM sucrose, 0.1 mM EGTA, 20 mM Tris–HCl (pH 7.4), 2.5 mM Pi and 1 mM MgCl2. (A) Hydrogen peroxide (ROS) production was assessed by Amplex Red and horse radish peroxidase; (B) NADH concentration was followed by determining its spontaneous autofluorescence. One typical experiment is presented.

References

  1. Fulda S, Gorman AM, Hori O, Samali A (2010) Cellular stress responses: cell survival and cell death. Int J Cell Biol. 2010;2010:214074. doi: 10.1155/2010/214074.
  2. Somayajulu-Niţu M, Sandhu JK, Cohen J, Sikorska M, Sridhar TS, Matei A, Borowy-Borowski H, Pandey S (2009) Paraquat induces oxidative stress, neuronal loss in substantia nigra region and parkinsonism in adult rats: neuroprotection and amelioration of symptoms by water-soluble formulation of coenzyme Q10. BMC Neurosci. 2009 Jul 27;10:88. doi: 10.1186/1471-2202-10-88.
  3. Kent M, Welladsen HM, Mangott A, Li Y (2015) Nutritional evaluation of Australian microalgae as potential human health supplements. PLoS One. 2015 Feb 27;10(2):e0118985. doi: 10.1371/journal.pone.0118985.

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