Testosterone Administration after Traumatic Brain Injury Reduces Mitochondrial Dysfunction and Neurodegeneration Article Swipe

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Randhall Bruce Carteri , Afonso Kopczynski , Marcelo Salimen Rodolphi , Nathan Ryzewski Strogulski , Mônia Sartor , Marceli Feldmann , Marco Antônio De Bastiani , Clóvis Milton Duval Wannmacher , Itiane Diehl de Franceschi , Gisele Hansel , Douglas H. Smith , Luis Valmor Portela ·

YOU? · · 2019 · Open Access · · DOI: https://doi.org/10.1089/neu.2018.6266

Traumatic brain injury (TBI) increases Ca²⁺ influx into neurons and desynchronizes mitochondrial function leading to energy depletion and apoptosis. This process may be influenced by brain testosterone (TS) levels, which are known to decrease after TBI. We hypothesized that a TS-based therapy could preserve mitochondrial neuroenergetics after TBI, thereby reducing neurodegeneration. C57BL/6J mice were submitted to sham treatment or severe parasagittal controlled cortical impact (CCI) and were subcutaneously injected with either vehicle (VEH-SHAM and VEH-CCI) or testosterone cypionate (15 mg/kg, TS-CCI) for 10 days. Cortical tissue homogenates ipsilateral to injury were used for neurochemical analysis. The VEH-CCI group displayed an increased Ca²⁺-induced mitochondrial swelling after the addition of metabolic substrates (pyruvate, malate, glutamate, succinate, and adenosine diphosphate [PMGSA]). The addition of Na⁺ stimulated mitochondrial Ca²⁺ extrusion through Na⁺/Ca²⁺/Li⁺ exchanger (NCLX) in VEH-SHAM and TS-CCI, but not in the VEH-CCI group. Reduction in Ca²⁺ efflux post-injury was associated with impaired mitochondrial membrane potential formation/dissipation, and decreased mitochondrial adenosine triphosphate (ATP)-synthase coupling efficiency. Corroborating evidence of mitochondrial uncoupling was observed with an increase in H₂O₂ production post-injury, but not in superoxide dismutase (SOD2) protein levels. TS administration significantly reduced these neuroenergetic alterations. At molecular level, TS prevented the increase in pTau^Ser396 and alpha-Spectrin fragmentation by the Ca²⁺dependent calpain-2 activation, and decreased both caspase-3 activation and Bax/BCL-2 ratio, which suggests a downregulation of mitochondrial apoptotic signals. Search Tool for the Retrieval of Interacting Genes/Proteins database provided two distinct gene/protein clusters, "upregulated and downregulated," interconnected through SOD2. Therefore, TS administration after a severe CCI improves the mitochondrial Ca²⁺extrusion through NCLX exchanger and ATP synthesis efficiency, ultimately downregulating the overexpression of molecular drivers of neurodegeneration.

Related Topics

Traumatic Brain Injury

Concepts

SOD2 Traumatic brain injury Endocrinology Internal medicine Mitochondrion Adenosine triphosphate Neurodegeneration MFN2 Mitochondrial biogenesis TFAM Biology Chemistry Superoxide dismutase Cell biology Medicine Oxidative stress mitochondrial fusion Biochemistry Mitochondrial DNA Disease Gene Psychiatry

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Type: article
Language: en
Landing Page: https://doi.org/10.1089/neu.2018.6266
OA Status: green
Cited By: 62
References: 61
Related Works: 10
OpenAlex ID: https://openalex.org/W2917117542

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OpenAlex ID: https://openalex.org/W2917117542

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DOI: https://doi.org/10.1089/neu.2018.6266

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Title: Testosterone Administration after Traumatic Brain Injury Reduces Mitochondrial Dysfunction and Neurodegeneration

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Type: article

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Language: en

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Publication year: 2019

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Publication date: 2019-02-22

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Authors: Randhall Bruce Carteri, Afonso Kopczynski, Marcelo Salimen Rodolphi, Nathan Ryzewski Strogulski, Mônia Sartor, Marceli Feldmann, Marco Antônio De Bastiani, Clóvis Milton Duval Wannmacher, Itiane Diehl de Franceschi, Gisele Hansel, Douglas H. Smith, Luis Valmor Portela

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Landing page: https://doi.org/10.1089/neu.2018.6266

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Open access: Yes

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OA status: green

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OA URL: https://www.ncbi.nlm.nih.gov/pmc/articles/6653807

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Concepts: SOD2, Traumatic brain injury, Endocrinology, Internal medicine, Mitochondrion, Adenosine triphosphate, Neurodegeneration, MFN2, Mitochondrial biogenesis, TFAM, Biology, Chemistry, Superoxide dismutase, Cell biology, Medicine, Oxidative stress, mitochondrial fusion, Biochemistry, Mitochondrial DNA, Disease, Gene, Psychiatry

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Cited by: 62

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Citations by year (recent): 2025: 12, 2024: 8, 2023: 9, 2022: 9, 2021: 15

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References (count): 61

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abstract_inverted_index.submitted	54
abstract_inverted_index.synthesis	259
abstract_inverted_index.treatment	57
abstract_inverted_index.(pyruvate,	110
abstract_inverted_index.Therefore,	243
abstract_inverted_index.activation	211
abstract_inverted_index.apoptosis.	18
abstract_inverted_index.associated	146
abstract_inverted_index.controlled	61
abstract_inverted_index.glutamate,	112
abstract_inverted_index.influenced	23
abstract_inverted_index.production	173
abstract_inverted_index.stimulated	122
abstract_inverted_index.substrates	109
abstract_inverted_index.succinate,	113
abstract_inverted_index.superoxide	178
abstract_inverted_index.ultimately	261
abstract_inverted_index.uncoupling	165
abstract_inverted_index.Interacting	229
abstract_inverted_index.activation,	206
abstract_inverted_index.diphosphate	116
abstract_inverted_index.efficiency,	260
abstract_inverted_index.efficiency.	160
abstract_inverted_index.homogenates	86
abstract_inverted_index.ipsilateral	87
abstract_inverted_index.post-injury	144
abstract_inverted_index."upregulated	237
abstract_inverted_index.alterations.	189
abstract_inverted_index.gene/protein	235
abstract_inverted_index.hypothesized	37
abstract_inverted_index.parasagittal	60
abstract_inverted_index.post-injury,	174
abstract_inverted_index.testosterone	26, 76
abstract_inverted_index.triphosphate	157
abstract_inverted_index.Corroborating	161
abstract_inverted_index.fragmentation	201
abstract_inverted_index.mitochondrial	11, 44, 102, 123, 149, 155, 164, 220, 252
abstract_inverted_index.neurochemical	93
abstract_inverted_index.significantly	185
abstract_inverted_index.(ATP)-synthase	158
abstract_inverted_index.Genes/Proteins	230
abstract_inverted_index.Na<sup>+</sup>	121
abstract_inverted_index.administration	184, 245
abstract_inverted_index.alpha-Spectrin	200
abstract_inverted_index.desynchronizes	10
abstract_inverted_index.downregulating	262
abstract_inverted_index.downregulation	218
abstract_inverted_index.interconnected	240
abstract_inverted_index.neuroenergetic	188
abstract_inverted_index.overexpression	264
abstract_inverted_index.subcutaneously	67
abstract_inverted_index.Ca<sup>2+</sup>	5, 124, 142
abstract_inverted_index.downregulated,"	239
abstract_inverted_index.neuroenergetics	45
abstract_inverted_index.neurodegeneration.	50, 269
abstract_inverted_index.pTau<sup>Ser396</sup>	198
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abstract_inverted_index.Ca<sup>2+</sup>-induced	101
abstract_inverted_index.Ca<sup>2+</sup>dependent	204
abstract_inverted_index.Ca<sup>2+</sup>extrusion	253
abstract_inverted_index.H<sub>2</sub>O<sub>2</sub>	172
abstract_inverted_index.Na<sup>+</sup>/Ca<sup>2+</sup>/Li<sup>+</sup>	127
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institutions_distinct_count	12
corresponding_institution_ids	https://openalex.org/I130442723
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