Antioxidant Effects of SelegilIne in Oxidative Stress Induced by Iron Neonatal Treatment in Rats

Budni, Patrícia; Lima, Maria Noêmia Martins de; Polydoro, Manuela; Moreira, José Cláudio Fonseca; Schröder, Nadja; Dal‐Pizzol, Felipe

doi:10.1007/s11064-006-9249-x

Cited by 18 publications

(10 citation statements)

References 58 publications

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“…Previous studies performed by our research group have shown that neonatal iron treatment induces lipid peroxidation and increases mitochondrial superoxide generation in the hippocampus, cortex, and substantia nigra 6,34 and protein carbonylation in the substantia nigra 35 in adult rats. In line with the present results, in previous studies we have also observed an increase in the apoptotic markers, Caspase 3 13 and Par4 12 in the brains of iron-treated rats.…”

Section: Discussionmentioning

confidence: 70%

Antiapoptotic effects of cannabidiol in an experimental model of cognitive decline induced by brain iron overload

et al. 2018

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Iron accumulation in the brain has been recognized as a common feature of both normal aging and neurodegenerative diseases. Cognitive dysfunction has been associated to iron excess in brain regions in humans. We have previously described that iron overload leads to severe memory deficits, including spatial, recognition, and emotional memory impairments in adult rats. In the present study we investigated the effects of neonatal iron overload on proteins involved in apoptotic pathways, such as Caspase 8, Caspase 9, Caspase 3, Cytochrome c, APAF1, and PARP in the hippocampus of adult rats, in an attempt to establish a causative role of iron excess on cell death in the nervous system, leading to memory dysfunction. Cannabidiol (CBD), the main non-psychotropic component of Cannabis sativa, was examined as a potential drug to reverse iron-induced effects on the parameters analyzed. Male rats received vehicle or iron carbonyl (30 mg/kg) from the 12th to the 14th postnatal days and were treated with vehicle or CBD (10 mg/kg) for 14 days in adulthood. Iron increased Caspase 9, Cytochrome c, APAF1, Caspase 3 and cleaved PARP, without affecting cleaved Caspase 8 levels. CBD reversed iron-induced effects, recovering apoptotic proteins Caspase 9, APAF1, Caspase 3 and cleaved PARP to the levels found in controls. These results suggest that iron can trigger cell death pathways by inducing intrinsic apoptotic proteins. The reversal of iron-induced effects by CBD indicates that it has neuroprotective potential through its anti-apoptotic action.

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Section: Discussionmentioning

confidence: 70%

Antiapoptotic effects of cannabidiol in an experimental model of cognitive decline induced by brain iron overload

et al. 2018

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“…Brain regional biochemical analyses in the 34 preclinical studies most frequently investigated oxidative stress, neurochemical markers, or iron levels. Markers of brain oxidative stress, including malondialdehyde and protein carbonyls, were increased in 9 studies 34 , 49 , 55–58 , 63–65 ; the 1 study that assessed glutathione levels found no change. 66 Six studies assessed the effects of neonatal iron intake on brain neurochemistry outcomes.…”

Section: Resultsmentioning

confidence: 95%

Impact of high iron intake on cognition and neurodegeneration in humans and in animal models: a systematic review

et al. 2017

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ContextAccumulation of brain iron is linked to aging and protein-misfolding neurodegenerative diseases. High iron intake may influence important brain health outcomes in later life.ObjectiveThe aim of this systematic review was to examine evidence from animal and human studies of the effects of high iron intake or peripheral iron status on adult cognition, brain aging, and neurodegeneration.Data SourcesMEDLINE, Scopus, CAB Abstracts, the Cochrane Central Register of Clinical Trials, and OpenGrey databases were searched.Study SelectionStudies investigating the effect of elevated iron intake at all postnatal life stages in mammalian models and humans on measures of adult brain health were included.Data ExtractionData were extracted and evaluated by two authors independently, with discrepancies resolved by discussion. Neurodegenerative disease diagnosis and/or behavioral/cognitive, biochemical, and brain morphologic findings were used to study the effects of iron intake or peripheral iron status on brain health. Risk of bias was assessed for animal and human studies. PRISMA guidelines for reporting systematic reviews were followed.ResultsThirty-four preclinical and 14 clinical studies were identified from database searches. Thirty-three preclinical studies provided evidence supporting an adverse effect of nutritionally relevant high iron intake in neonates on brain-health-related outcomes in adults. Human studies varied considerably in design, quality, and findings; none investigated the effects of high iron intake in neonates/infants.ConclusionsHuman studies are needed to verify whether dietary iron intake levels used in neonates/infants to prevent iron deficiency have effects on brain aging and neurodegenerative disease outcomes.

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“…Previous studies proposed that selegiline, a selective irreversible MAO-B inhibitor, is able to reduce the TBARS levels in rat brain tissue ( 37 , 38 ) . In the present study, it was demonstrated that there is a positive correlation between brain MAO activity and lipid peroxidation of brain and liver (Table 3).…”

Section: Discussionmentioning

confidence: 99%

Both inorganic and organic selenium supplements can decrease brain monoamine oxidase B enzyme activity in adult rats

2008

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It has been observed that the levels of brain monoamine oxidase B (MAO-B) increase during ageing. MAO catalyses the oxidative deamination of neurotransmitters, in which the by-product H2O2 is subsequently generated. Se exists naturally in inorganic and organic forms and is considered to play a key role in antioxidation functioning. The objective of the present study was to investigate two chemical forms of Se compounds for their inhibition effect on rat brain MAO-B. The total antioxidant capacity and lipid peroxidation of rats were also examined. The rats (age 7 weeks) were divided into four groups: the control group, tocopherol group (T group, positive control), selenite group (SE group, representing the inorganic Se group) and seleno-yeast group (SY group, representing the organic Se group). The rats were fed for 11 weeks with normal diets and 12 weeks with test diets. The serum total antioxidant capacity of the SE and SY groups was significantly higher than that in the control and T groups. In rat brains and livers, the lipid peroxidation levels were significantly decreased in the T, SE and SY groups. MAO-B activity showed a significant decrease in the T, SE and SY groups in rat brains but no significant change could be noted in the rat livers. In conclusion, the present study indicates that inorganic or organic Se supplementation can decrease the brain MAO-B enzyme activity in adult rats and can be accomplished by the effect of the Se antioxidation capability.

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Antioxidant Effects of SelegilIne in Oxidative Stress Induced by Iron Neonatal Treatment in Rats

Cited by 18 publications

References 58 publications

Antiapoptotic effects of cannabidiol in an experimental model of cognitive decline induced by brain iron overload

Antiapoptotic effects of cannabidiol in an experimental model of cognitive decline induced by brain iron overload

Impact of high iron intake on cognition and neurodegeneration in humans and in animal models: a systematic review

Both inorganic and organic selenium supplements can decrease brain monoamine oxidase B enzyme activity in adult rats

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