Effects of hydrogen gas inhalation on L-DOPA-induced dyskinesia
Nascimento GC, Santos BM, Pedrazzi JF, Silva-Amaral D, Bortolanza M, Harris GT, Del Bel E, Branco LGS. · Brain, Behavior, & Immunity - Health. 2023;30:100623.
Study at a glance
Preclinical
Rats with unilateral 6-hydroxydopamine lesions used as a preclinical model of Parkinsonian motor impairment and L-DOPA-induced dyskinesia.
After 15 days of chronic L-DOPA 20 mg/kg plus benserazide 5 mg/kg, rats inhaled the test gas for 1 hour immediately before the final L-DOPA dose and behavioral testing. · 2% H₂, 21% O₂ and balance N₂ at a reported total flow of 2.4 L/min; an air-mixture control contained 0% H₂, 21% O₂ and balance N₂. H₂ concentration was monitored with a gas analyzer.
A single 1-hour H₂ exposure before the last dose in the 15-day L-DOPA protocol; dyskinesia was observed for 120 minutes and tissues/cytokines were assessed afterward.
The article reports about 48% lower abnormal-involuntary-movement scores with H₂ and no impairment of L-DOPA-restored locomotor activity. Microglial number/reactivity and several pro-inflammatory cytokines were lower, while IL-10 was higher. Astrocyte cell number and morphology, microglial process intersections and several control-group comparisons were not significantly changed.
Preclinical model, small assay-specific groups, a single H₂ exposure immediately before the final L-DOPA dose and many behavioral, cellular and cytokine outcomes. It does not show treatment of Parkinson's disease or dyskinesia in people. Brazilian CNPq and FAPESP grants supported the work; authors declared no competing financial interests or personal relationships.
What kind of evidence is this?
Preclinical
Controlled 6-hydroxydopamine rat experiment after chronic L-DOPA treatment
Parkinson’s disease
Inhaled H₂
Information not yet classified
Some editorial classification fields are still pending. The source-reported outcomes and result are shown below; Hydrogenology does not infer a positive or negative signal from prose automatically.
Methods
Rats with unilateral 6-hydroxydopamine lesions used as a preclinical model of Parkinsonian motor impairment and L-DOPA-induced dyskinesia.
The behavioral experiment used 42 rats (reported group sizes n=5–6); histology used 23 rats (n=7–8) and the separate cytokine experiment used 22 rats (n=7–8). The article does not present these assay cohorts as one consolidated sample.
A single 1-hour H₂ exposure before the last dose in the 15-day L-DOPA protocol; dyskinesia was observed for 120 minutes and tissues/cytokines were assessed afterward.
After 15 days of chronic L-DOPA 20 mg/kg plus benserazide 5 mg/kg, rats inhaled the test gas for 1 hour immediately before the final L-DOPA dose and behavioral testing.
H₂ diluted in a normoxic nitrogen/oxygen carrier — H₂ alone was the added test gas, not Brown's gas.
2% H₂, 21% O₂ and balance N₂ at a reported total flow of 2.4 L/min; an air-mixture control contained 0% H₂, 21% O₂ and balance N₂. H₂ concentration was monitored with a gas analyzer.
48 mL/min H₂, calculated from the reported 2,400 mL/min total flow × 2% H₂.
21% O₂; 504 mL/min O₂, calculated from 2,400 mL/min × 21%. The remaining carrier was approximately 1,848 mL/min N₂.
Matched air mixture containing 0% H₂, 21% O₂ and balance N₂ at the same 2.4 L/min flow, across sham, lesion, vehicle and L-DOPA conditions.
Outcomes and reported result
Axial, limb and orofacial abnormal involuntary movements, locomotor activity, striatal microglial and astrocyte morphology, plasma and striatal cytokines and correlations between cytokines and dyskinesia scores.
The article reports about 48% lower abnormal-involuntary-movement scores with H₂ and no impairment of L-DOPA-restored locomotor activity. Microglial number/reactivity and several pro-inflammatory cytokines were lower, while IL-10 was higher. Astrocyte cell number and morphology, microglial process intersections and several control-group comparisons were not significantly changed.
The complete open-access PMC/Elsevier article, gas chamber protocol, concentration and total flow, behavioral, histology and cytokine cohorts, positive and null results, funding and conflict statement were checked.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Preclinical model, small assay-specific groups, a single H₂ exposure immediately before the final L-DOPA dose and many behavioral, cellular and cytokine outcomes. It does not show treatment of Parkinson's disease or dyskinesia in people. Brazilian CNPq and FAPESP grants supported the work; authors declared no competing financial interests or personal relationships.
6-OHDA-lesioned rats receiving chronic L-DOPA; not clinical evidence in people with Parkinson's disease.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 37096172 · DOI: 10.1016/j.bbih.2023.100623
Open-access publisher article and PubMed Central copy.
Complete PubMed Central/Elsevier article and PubMed metadata; full-text extraction checked 8 August 2026.
10 August 2026
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