Melatonin's antioxidant protection against δ‐aminolevulinic acid‐induced oxidative damage in rat cerebellum

Princ, Fernando G.; Juknat, Adela Ana; Maxit, Andrea Grisel; Cardalda, Carina; Battle, Alcira

doi:10.1111/j.1600-079x.1997.tb00333.x

Cited by 44 publications

(32 citation statements)

References 35 publications

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“…Taking into account the fact that oxidative stress is a condition referred to as an imbalance between oxidant generation and antioxidant defense systems, which GSH is a leading substrate for enzymatic antioxidant functions and it is also a known radical scavenger, its precursor SAM would be acting as an antioxidant. This explanation could also be extended to ALA toxicity, because ALA accumulation generates ROS (Princ et al 1997;1998;Reiter and Tyrrel 2000) and it has been shown that SAM was capable of counteracting this effect (Paredes et al 1987). Our results clearly demonstrated that in all tissues of Cd 2+ treated plants there is accumulation of ALA as well as diminution of PBG content as a result of ALA-D activity inhibition.…”

Section: Discussionsupporting

confidence: 49%

Cadmium induced oxidative stress in soybean plants also by the accumulation of δ-aminolevulinic acid

et al. 2007

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Cadmium toxicity has been extensively studied in plants, however its biochemical mechanism of action has not yet been well established. To fulfil this objective, four-weeks-old soybean nodulated plants were treated with 200 muM Cd(2+) for 48 h. delta-aminolevulinic acid dehydratase (ALA-D, E.C. 4.2.1.24) activity and protein expression, as well as delta-aminolevulinic acid (ALA) and porphobilinogen (PBG) concentrations were determined in nodules, roots and leaves. In vitro experiments carried out in leaves were performed using leaf discs to evaluate the oxidant and antioxidant properties of ALA and S-adenosyl-L: -methinone (SAM), respectively. Oxidative stress parameters such as thiobarbituric acid reactive substances (TBARS) and GSH levels as well as superoxide dismutase (SOD, E.C. 1.15.1.1), and guaiacol peroxidase (GPOX, E.C. 1.11.1.7) were also determined. Cadmium treatment caused 100% inhibition of ALA-D activity in roots and leaves, and 72% inhibition in nodules whereas protein expression remained unaltered in the three studied tissues. Plants accumulated ALA in nodules (46%), roots (2.5-fold) and leaves (104%), respect to controls. From in vitro experiments using leaf discs, exposed to ALA or Cd(2+), it was found that TBARS levels were enhanced, while GSH content and SOD and GPOX activities and expressions were diminished. The protective role of SAM against oxidative stress generated by Cd(2+) and ALA was also demonstrated. Data presented in this paper let us to suggest that accumulation of ALA in nodules, roots and leaves of soybean plants due to treatment with Cd(2+) is highly responsible for oxidative stress generation in these tissues.

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Section: Discussionsupporting

confidence: 49%

Cadmium induced oxidative stress in soybean plants also by the accumulation of δ-aminolevulinic acid

et al. 2007

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“…The cerebellum, which is a target of melatonin G-protein coupled receptors [37]–[40], was used as a classical model to study the protective effect of melatonin against hyperbaric oxygen exposure [41], lipid peroxidation [42], [43], glutamate-induced neurotoxicity [44], aluminum exposition [45] and hypoxia [46]. Melatonin was shown to interfere with cerebellar tissue by inhibiting glutamate release [47], the transient outward flow of potassium [48], nicotinic currents [49] and the migration of granule cells [50].…”

Section: Discussionmentioning

confidence: 99%

The Cellular State Determines the Effect of Melatonin on the Survival of Mixed Cerebellar Cell Culture

Franco

Markus

2014

PLoS ONE

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The constitutive activation of nuclear factor-κB (NF-κB), a key transcription factor involved in neuroinflammation, is essential for the survival of neurons in situ and of cerebellar granule cells in culture. Melatonin is known to inhibit the activation of NF-κB and has a cytoprotective function. In this study, we evaluated whether the cytoprotective effect of melatonin depends on the state of activation of a mixed cerebellar culture that is composed predominantly of granule cells; we tested the effect of melatonin on cultured rat cerebellar cells stimulated or not with lipopolysaccharide (LPS). The addition of melatonin (0.1 nM–1 µM) reduced the survival of naïve cells while inhibiting LPS-induced cell death. Melatonin (100 nM) transiently (15 min) inhibited the nuclear translocation of both NF-κB dimers (p50/p50, p50/RelA) and, after 60 min, increased the activation of p50/RelA. Melatonin-induced p50/RelA activity in naïve cells resulted in the transcription of inducible nitric oxide synthase (iNOS) and the production of NO. Otherwise, in cultures treated with LPS, melatonin blocked the LPS-induced activation of p50/RelA and the reduction in p50/p50 levels and inhibited iNOS expression and NO synthesis. Therefore, melatonin in vehicle-treated cells induces cell death, while it protects against LPS-induced cytotoxicity. In summary, we confirmed that melatonin is a neuroprotective drug when cerebellar cells are challenged; however, melatonin can also lead to cell death when the normal balance of the NF-κB pathway is disturbed. Our data provide a mechanistic basis for understanding the influence of cell context on the final output response of melatonin.

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“…To name only a few, melatonin has been successfully used to reduce neural damage during drug-induced excitotoxicity [182], models of Alzheimer's disease [183], models of Parkinson's disease, [184] nitric oxide neurotoxicity and ischemia-reperfusion injury [185], acute intermittent porphyria [186], lipopolysaccharide exposure [187], and hyperbaric oxygen exposure [188]. In peripheral organs as well, melatonin has proven highly effective in combatting cellular and tissue damage due to oxidative stress [170,171,174,189,190].…”

Section: The Utility Of Melatonin As a Pharmacological Agent In Oxidamentioning

confidence: 99%

Prospects of the Clinical Utilization of Melatonin

Bubenik

Blask

Brown

et al. 1998

Biol Signals Recept

129

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This review summarizes the present knowledge on melatonin in several areas on physiology and discusses various prospects of its clinical utilization. Ever increasing evidence indicates that melatonin has an immuno-hematopoietic role. In animal studies, melatonin provided protection against gram-negative septic shock, prevented stress-induced immunodepression, and restored immune function after a hemorrhagic shock. In human studies, melatonin amplified the antitumoral activity of interleukin-2. Melatonin has been proven as a powerful cytostatic drug in vitro as well as in vivo. In the human clinical field, melatonin appears to be a promising agent either as a diagnostic or prognostic marker of neoplastic diseases or as a compound used either alone or in combination with the standard cancer treatment. Utilization of melatonin for treatment of rhythm disorders, such as those manifested in jet lag, shift work or blindness, is one of the oldest and the most successful clinical application of this chemical. Low doses of melatonin applied in controlled-release preparation were very effective in improving the sleep latency, increasing the sleep efficiency and rising sleep quality scores in elderly, melatonin-deficient insomniacs. In the cardiovascular system, melatonin seems to regulate the tone of cerebral arteries; melatonin receptors in vascular beds appear to participate in the regulation of body temperature. Heat loss may be the principal mechanism in the initiation of sleepiness caused by melatonin. The role of melatonin in the development of migraine headaches is at present uncertain but more research could result in new ways of treatment. Melatonin is the major messenger of light-dependent periodicity, implicated in the seasonal reproduction of animals and pubertal development in humans. Multiple receptor sites detected in brain and gonadal tissues of birds and mammals of both sexes indicate that melatonin exerts a direct effect on the vertebrate reproductive organs. In a clinical study, melatonin has been used successfully as an effective female contraceptive with little side effects. Melatonin is one of the most powerful scavengers of free radicals. Because it easily penetrates the blood-brain barrier, this antioxidant may, in the future, be used for the treatment of Alzheimer’s and Parkinson’s diseases, stroke, nitric oxide, neurotoxicity and hyperbaric oxygen exposure. In the digestive tract, melatonin reduced the incidence and severity of gastric ulcers and prevented severe symptoms of colitis, such as mucosal lesions and diarrhea.

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Melatonin's antioxidant protection against δ‐aminolevulinic acid‐induced oxidative damage in rat cerebellum

Cited by 44 publications

References 35 publications

Cadmium induced oxidative stress in soybean plants also by the accumulation of δ-aminolevulinic acid

Cadmium induced oxidative stress in soybean plants also by the accumulation of δ-aminolevulinic acid

The Cellular State Determines the Effect of Melatonin on the Survival of Mixed Cerebellar Cell Culture

Prospects of the Clinical Utilization of Melatonin

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