Differential effects of alprazolam against methylphenidate-induced neurobehavioral alterations

Dutt, Meenu; Dharavath, Ravinder Naik; Kaur, Tarundeep; Chopra, Kanwaljit; Sharma, Shweta

doi:10.1016/j.physbeh.2020.112935

Cited by 10 publications

(3 citation statements)

References 45 publications

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“…Finally, acute administration of high doses of MPH in adult rats produced oxidative damage, reduced GSH, SOD, GPx, and glutathione reductase (GR) activities, and provoked neurodegeneration in the cerebral cortex and hippocampus [ 79 ]. Recently, in the cortex and hippocampus of rats treated with MPH, MDA levels were increased and SOD levels reduced [ 81 ].…”

Section: Role Of Oxidative Stressmentioning

confidence: 99%

Role of Oxidative Stress and Neuroinflammation in Attention-Deficit/Hyperactivity Disorder

Corona

2020

Antioxidants

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Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder of childhood. Although abnormalities in several brain regions and disturbances of the catecholaminergic pathway have been demonstrated, the pathophysiology of ADHD is not completely understood, but as a multifactorial disorder, has been associated with an increase in oxidative stress and neuroinflammation. This review presents an overview of factors that increase oxidative stress and neuroinflammation. The imbalance between oxidants and antioxidants and also the treatment with medications are two factors that can increase oxidative damage, whereas the comorbidity between ADHD and inflammatory disorders, altered immune response, genetic and environmental associations, and polymorphisms in inflammatory-related genes can increase neuroinflammation. Evidence of an association with these factors has become valuable for research on ADHD. Such evidence opens up new intervention routes for the use of natural products as antioxidants that could have potential as a treatment against oxidative stress and neuroinflammation in ADHD.

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Section: Role Of Oxidative Stressmentioning

confidence: 99%

Role of Oxidative Stress and Neuroinflammation in Attention-Deficit/Hyperactivity Disorder

Corona

2020

Antioxidants

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“…Moreover, the drugs used to treat ADHD may cause the accumulation of catecholamines, leading to enhanced autoxidation and oxidative stress (Martins et al, 2006;Corona, 2020). For instance, MPH administration reduced SOD, GSH, GPx and glutathione reductase activities in rats, resulting in oxidative stress and neurodegeneration (Motaghinejad et al, 2017;Dutt et al, 2020). Alternatively, PIO has been shown to reduce oxidative stress by upregulating antioxidant pathways (Corona and Duchen, 2016).…”

Section: Discussionmentioning

confidence: 99%

Pioglitazone enhances brain mitochondrial biogenesis and phase II detoxification capacity in neonatal rats with 6-OHDA-induced unilateral striatal lesions

Vázquez-González

Corona

2023

Front. Neurosci.

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The psychostimulant methylphenidate (MPH) is the first-line pharmacological treatment for attention-deficit/hyperactivity disorder (ADHD), but has numerous adverse side effects. The PPARγ receptor agonist pioglitazone (PIO) is known to improve mitochondrial bioenergetics and antioxidant capacity, both of which may be deficient in ADHD, suggesting utility as an adjunct therapy. Here, we assessed the effects of PIO on ADHD-like symptoms, mitochondrial biogenesis and antioxidant pathways in multiple brain regions of neonate rats with unilateral striatal lesions induced by 6-hydroxydopamine (6-OHDA) as an experimental ADHD model. Unilateral striatal injection of 6-OHDA reduced ipsilateral dopaminergic innervation by 33% and increased locomotor activity. This locomotor hyperactivity was not altered by PIO treatment for 14 days. However, PIO increased the expression of proteins contributing to mitochondrial biogenesis in the striatum, hippocampus, cerebellum and prefrontal cortex of 6-OHDA-lesioned rats. In addition, PIO treatment enhanced the expression of the phase II transcription factor Nrf2 in the striatum, prefrontal cortex and cerebellum. In contrast, no change in the antioxidant enzyme catalase was observed in any of the brain regions analyzed. Thus, PIO may improve mitochondrial biogenesis and phase 2 detoxification in the ADHD brain. Further studies are required to determine if different dose regimens can exert more comprehensive therapeutic effects against ADHD neuropathology and behavior.

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“…When co-administered with other depressant agents such as ethanol, alprazolam becomes particularly toxic, causing behavioral irritability and aggression (Huang et al, 2018). Chronic administration of alprazolam alone or with central nervous (CNS) stimulants increases oxidative stress and inflammation in the brain and induces neurobehavioral, histopathological and neurotransmitters levels' alterations (Dutt et al, 2020a). By means of spectrophotometry, alprazolam was shown to bind with hemoglobin (Hb), altering the α-helical structure of Hb-subunits.…”

Section: Introductionmentioning

confidence: 99%

Modification of alprazolam-induced liver injury by bone marrow-derived mesenchymal stem cells and the role of miRNA-192

Labib¹

2022

EJA

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The group of drugs known as Benzodiazepines (BDZs) are among the most widely prescribed CNS-depressant drugs. Alprazolam (Alp) is a member of the BDZs family, commonly prescribed as an antipsychotic and anxiolytic agent. Induction of oxidative stress, impairment of cognitive functions and psychomotor skills, conformational alterations in hemoglobin structure and elevation of liver enzymes are among the side effects reported on the use of alprazolam. Several studies have found that alprazolam could favor hepatotoxicity, whereas other studies contradicted those findings. Bone marrow-derived mesenchymal stem cells (BM-MSCs) have been studied as a novel approach for treatment of liver diseases. The current study was designed to assess the biochemical, histopathological and molecular liver alterations in response to oral administration of alprazolam at a dose of 0.3 mg/kg/day for 4 weeks in adult male albino rats and to evaluate the therapeutic effect of BM-MSCs on the alprazolam- induced alterations. Forty adult male albino rats (Sprague Dawley strain; 170-200 g mean body weight) were used. Liver enzymes were measured, isolation and preparation of BM- MSCs were done, and immunohistochemical staining for alpha smooth muscle actin and FGF2 were assessed. Moreover, histological and ultrastructural liver tissue examination and PCR detection of SOD, TNF-α and mirNA-192 were investigated. Animals exposed to alprazolam developed liver injury characterized by significant increase in TNF-α and significant decrease in SOD and miRNA- 192 expression. Histological findings provided supportive evidence for the biochemical and molecular analyses. Treatment with stem cells caused a significant alleviation of the alprazolam- induced findings. In conclusion, alprazolam was found to induce liver injury and oxidative stress, which were ameliorated by BM-MSCs administration.

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Differential effects of alprazolam against methylphenidate-induced neurobehavioral alterations

Cited by 10 publications

References 45 publications

Role of Oxidative Stress and Neuroinflammation in Attention-Deficit/Hyperactivity Disorder

Role of Oxidative Stress and Neuroinflammation in Attention-Deficit/Hyperactivity Disorder

Pioglitazone enhances brain mitochondrial biogenesis and phase II detoxification capacity in neonatal rats with 6-OHDA-induced unilateral striatal lesions

Modification of alprazolam-induced liver injury by bone marrow-derived mesenchymal stem cells and the role of miRNA-192

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