PMID- 37891966
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231030
IS  - 2076-3921 (Print)
IS  - 2076-3921 (Electronic)
IS  - 2076-3921 (Linking)
VI  - 12
IP  - 10
DP  - 2023 Oct 20
TI  - Effects of Acetyl-L-Carnitine on Oxidative Stress in Amyotrophic Lateral 
      Sclerosis Patients: Evaluation on Plasma Markers and Members of the Neurovascular 
      Unit.
LID - 10.3390/antiox12101887 [doi]
LID - 1887
AB  - Oxidative stress, the alteration of mitochondrial function, and the neurovascular 
      unit (NVU), play a role in Amyotrophic Lateral Sclerosis (ALS) pathogenesis. We 
      aimed to demonstrate the changes in the plasma redox system and nitric oxide (NO) 
      in 32 new ALS-diagnosed patients in treatment with Acetyl-L-Carnitine (ALCAR) 
      compared to healthy controls. We also evaluated the effects of plasma on human 
      umbilical cord-derived endothelial vascular cells (HUVEC) and astrocytes. The 
      analyses were performed at the baseline (T0), after three months (T1), and after 
      six months (T2). In ALS patients at T0/T1, the plasma markers of lipid 
      peroxidation, thiobarbituric acid reactive substances (TBARS) and 4-hydroxy 
      nonenal (4-HNE) were higher, whereas the antioxidants, glutathione (GSH) and the 
      glutathione peroxidase (GPx) activity were lower than in healthy controls. At T2, 
      plasma TBARS and 4-HNE decreased, whereas plasma GSH and the GPx activity 
      increased in ALS patients. As regards NO, the plasma levels were firmly lower at 
      T0-T2 than those of healthy controls. Cell viability, and mitochondrial membrane 
      potential in HUVEC/astrocytes treated with the plasma of ALS patients at T0-T2 
      were reduced, while the oxidant release increased. Those results, which confirmed 
      the fundamental role of oxidative stress, mitochondrial function, and of the NVU 
      in ALS pathogenesis, can have a double meaning, acting as disease markers at 
      baseline and potential markers of drug effects in clinical practice and during 
      clinical trials.
FAU - Grossini, Elena
AU  - Grossini E
AUID- ORCID: 0000-0002-3012-259X
AD  - Laboratory of Physiology, Department of Translational Medicine, Universita del 
      Piemonte Orientale, 28100 Novara, Italy.
FAU - De Marchi, Fabiola
AU  - De Marchi F
AUID- ORCID: 0000-0003-0197-1880
AD  - ALS Center, Neurology Unit, Department of Translational Medicine, Universita del 
      Piemonte Orientale, 28100 Novara, Italy.
FAU - Venkatesan, Sakthipriyan
AU  - Venkatesan S
AUID- ORCID: 0000-0002-7517-2574
AD  - Laboratory of Physiology, Department of Translational Medicine, Universita del 
      Piemonte Orientale, 28100 Novara, Italy.
FAU - Mele, Angelica
AU  - Mele A
AD  - ALS Center, Neurology Unit, Department of Translational Medicine, Universita del 
      Piemonte Orientale, 28100 Novara, Italy.
FAU - Ferrante, Daniela
AU  - Ferrante D
AUID- ORCID: 0000-0003-4929-3759
AD  - Statistic Unit, Department of Translational Medicine, Universita del Piemonte 
      Orientale, 28100 Novara, Italy.
FAU - Mazzini, Letizia
AU  - Mazzini L
AD  - ALS Center, Neurology Unit, Department of Translational Medicine, Universita del 
      Piemonte Orientale, 28100 Novara, Italy.
LA  - eng
PT  - Journal Article
DEP - 20231020
PL  - Switzerland
TA  - Antioxidants (Basel)
JT  - Antioxidants (Basel, Switzerland)
JID - 101668981
PMC - PMC10604350
OTO - NOTNLM
OT  - astrocytes
OT  - disease progression
OT  - glutathione
OT  - mitochondria
OT  - nitric oxide
OT  - oxidants
OT  - vascular endothelial cells
COIS- The authors declare no conflict of interest.
EDAT- 2023/10/28 11:47
MHDA- 2023/10/28 11:48
PMCR- 2023/10/20
CRDT- 2023/10/28 01:01
PHST- 2023/10/09 00:00 [received]
PHST- 2023/10/19 00:00 [accepted]
PHST- 2023/10/28 11:48 [medline]
PHST- 2023/10/28 11:47 [pubmed]
PHST- 2023/10/28 01:01 [entrez]
PHST- 2023/10/20 00:00 [pmc-release]
AID - antiox12101887 [pii]
AID - antioxidants-12-01887 [pii]
AID - 10.3390/antiox12101887 [doi]
PST - epublish
SO  - Antioxidants (Basel). 2023 Oct 20;12(10):1887. doi: 10.3390/antiox12101887.