Melatonin and pinoline prevent aluminium-induced lipid peroxidation in rat synaptosomes

Millán-Plano, Sergio; García, Joaquín J.; Martı́nez-Balları́n, Enrique; Reíter, Russel J.; Ortega‐Gutiérrez, Santiago; Lázaro, Rosa Maria; Escanero, J.F.

doi:10.1016/s0946-672x(03)80044-5

Cited by 21 publications

(22 citation statements)

References 45 publications

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“…In the human CP brain, the presence of free radical injury is supported by the existence of both oxidative and nitrative stress markers of lipid peroxidation and nitrosylation/nitration, respectively (Haynes et al, 2003). LPS has been shown to cause the depletion of intracellular GSH and an increase in MDA, a byproduct of lipid peroxidation (Millan-Plano et al, 2003;Topal et al, 2004). This LPS-induced oxidativestress and lipid peroxidation leads to the production of potentially toxic aldehydes such as 4-HNE in the cell (Siems et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide-induced peroxisomal dysfunction exacerbates cerebral white matter injury: Attenuation by N-acetyl cysteine

Paintlia

Contreras

et al. 2008

Experimental Neurology

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Cerebral white matter injury during prenatal maternal infection characterized as periventricular leukomalacia (PVL) is the main substrate for cerebral palsy (CP) in premature infants. Previously, we reported that maternal LPS exposure causes oligodendrocyte (OL)-injury/hypomyelination in the developing brain which can be attenuated by an antioxidant agent, N-acetyl cysteine (NAC). Herein, we elucidated the role of peroxisomes in LPS-induced neuroinflammation and cerebral white matter injury. Peroxisomes are important for detoxification of reactive oxidative species (ROS) and metabolism of myelin-lipids in OLs. Maternal LPS exposure induced selective depletion of developing OLs in the fetal brain which was associated with ROS generation, glutathione depletion and peroxisomal dysfunction. Likewise, hypomyelination in the postnatal brain was associated with decrease in peroxisomes in OLs after maternal LPS exposure. Conversely, NAC abolished these LPS-induced effects in the developing brain. CP brains imitated these changes in peroxisomal/myelin proteins in the postnatal brain after maternal LPS exposure. In vitro studies revealed that proinflammatory cytokines cause OL-injury via peroxisomal dysfunction and ROS generation. NAC or WY14643 (peroxisome proliferators activated receptor (PPAR)-α agonist) reverses these effects of proinflammatory cytokines in the wild-type OLs, but not in PPAR-α (−/−) OLs. Similarly treated B12 oligodenroglial cells co-transfected with PPAR-α siRNAs/pTK-PPREx3-Luc, and LPS exposed PPAR-α (−/−) pregnant mice treated with NAC or WY14643 further suggested that PPAR-α activity mediates NAC-induced protective effects. Collectively, these data provide unprecedented evidence that LPS-induced peroxisomal dysfunction exacerbates cerebral white matter injury and NACinduced protection is via a PPAR-α dependent mechanism expands therapeutic avenues for PVL and related demyelinating diseases.

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Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide-induced peroxisomal dysfunction exacerbates cerebral white matter injury: Attenuation by N-acetyl cysteine

Paintlia

Contreras

et al. 2008

Experimental Neurology

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“…In the current study, we have investigated and compared the protective effects of melatonin and structurally-related compounds in preventing oxidative damage to lipids and proteins in membranes isolated from the whole brain. The in vitro model for induction of radical species via the Fenton reaction used a combination of FeCl 3 plus ascorbic acid, which is widely accepted in the field of oxidative stress research [23,24]. Lipid peroxidation was assessed by measuring the concentrations of malondialdehyde (MDA) and 4-hydroxyalkenals (4-HDA) and protein oxidation was monitored using methods based on carbonylation.…”

Section: Introductionmentioning

confidence: 99%

Melatonin and Structurally-Related Compounds Protect Synaptosomal Membranes from Free Radical Damage

Millán-Plano

Piedrafita

Miana-Mena

et al. 2010

IJMS

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Since biological membranes are composed of lipids and proteins we tested the in vitro antioxidant properties of several indoleamines from the tryptophan metabolic pathway in the pineal gland against oxidative damage to lipids and proteins of synaptosomes isolated from the rat brain. Free radicals were generated by incubation with 0.1 mM FeCl3, and 0.1 mM ascorbic acid. Levels of malondialdehyde (MDA) plus 4-hydroxyalkenal (4-HDA), and carbonyl content in the proteins were measured as indices of oxidative damage to lipids and proteins, respectively. Pinoline was the most powerful antioxidant evaluated, with melatonin, N-acetylserotonin, 5-hydroxytryptophan, 5-methoxytryptamine, 5-methoxytryptophol, and tryptoline also acting as antioxidants.

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“…However, excessive and prolonged aluminum exposure, e.g. of patients with chronic renal failure undergoing long-term hemodialysis that use solutions with aluminum or who received antiacids containing aluminum is directly related to dementia and other neurological disorders (Exley 1998;Millan-Plano et al 2003). Furthermore, aluminum accumulated in the liver can be toxic at high concentration (Wilhelm 1996).…”

Section: Introductionmentioning

confidence: 99%

“…Aluminum chloride was found to be embryotoxic and teratogenic when given parenterally to animals (Crammer et al 1986). Blood aluminum levels increase with age and moreover high aluminum concentration and lipid peroxidation processes are reportedly involved in the pathogenesis of Alzheimer's disease (Millan-Plano et al 2003).…”

Section: Introductionmentioning

confidence: 99%

Amelioration of aluminum toxicity with black seed supplement on rats

Mahdy

Farrag

2009

Toxicological & Environmental Chemistry

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The possible ameliorative effect of black seed (Nigella sativa L.) on aluminum chloride (AlCl 3 ) toxicity in rats was investigated. Thirty-two male rats were divided into four groups, eight rats each. Group 1 was served as a control group; group 2 was fed on diet supplemented with black seed, while groups 3 and 4 were fed on AlCl 3 (726 mg kg À1 b.w.) with or without black seed supplementation for six weeks. Blood and tissue samples were taken for hematological, biochemical, and histopathological studies. The results revealed that serum of AlCl 3 -fed rats exhibit a significant elevation in transaminases, urea, creatinine, total cholesterol and triglycerides in serum, while significant decreases in hemoglobin concentration and red blood cell count were recorded. Histopathological observations showed severe damage in the liver and kidneys. Co-administration of black seed to the AlCl À 3 treated group showed marked improvement in biochemical and histopathological findings as well as reduction of the damaged areas. These results indicate the protective effect of black seed against AlCl 3 -induced toxicity in rats.

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Melatonin and pinoline prevent aluminium-induced lipid peroxidation in rat synaptosomes

Cited by 21 publications

References 45 publications

Lipopolysaccharide-induced peroxisomal dysfunction exacerbates cerebral white matter injury: Attenuation by N-acetyl cysteine

Lipopolysaccharide-induced peroxisomal dysfunction exacerbates cerebral white matter injury: Attenuation by N-acetyl cysteine

Melatonin and Structurally-Related Compounds Protect Synaptosomal Membranes from Free Radical Damage

Amelioration of aluminum toxicity with black seed supplement on rats

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