Melatonin protects against lipid peroxidation induced by δ-aminolevulinic acid in rat cerebellum, cortex and hippocampus

Carneiro, R C G; Reíter, Russel J.

doi:10.1016/s0306-4522(97)00262-5

Cited by 60 publications

(35 citation statements)

References 41 publications

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“…Conversely, melatonin has been widely reported as a potent antioxidant (Marshall et al, 1996;Reiter et al, 1997;) that protects against LPO (Carneiro and Reiter, 1998) and increases both activity and expression of antioxidant enzymes (Rodriguez et al, 2004). Therefore, the age-related decrease in melatonin levels may contribute to aging process.…”

Section: Discussionmentioning

confidence: 99%

Aging affects oxidative state in hippocampus, hypothalamus and adrenal glands of Wistar rats

Siqueira

Fochesatto²,

Torres³

et al. 2005

Life Sciences

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Section: Discussionmentioning

confidence: 99%

Aging affects oxidative state in hippocampus, hypothalamus and adrenal glands of Wistar rats

Siqueira

Fochesatto²,

Torres³

et al. 2005

Life Sciences

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“…In our experimental model, melatonin, 6-hydroxymelatonin or N-acetylserotonin was intraperitoneally administered to the rats at a dose of 10 mg/kg body weight 30 min before the ANIT injection and 6, 12, and 18 h after ANIT The number of polymorphonuclear neutrophils and apoptotic cells were assayed in control rats (C), rats injected with melatonin (MEL), 6-hydroxymelatonin injection. This experimental injection schedule for melatonin and related indoles has been used in other experimental models and been found effective in reducing oxidative damage [Sewerynek et al, 1995;Carneiro and Reiter, 1998]. Melatonin, and to a lesser degree 6-hydroxymelatonin, as able to protect against ANIT-induced liver injury with cholestasis as demonstrated by the serum values of both SGPT and SGOT activities and total bilirubin concentration.…”

Section: Discussionmentioning

confidence: 99%

“…Groups I (control) and V (ANIT) received the dose intraperitoneally and at the same time the same volume of ethanol/saline solution. This scheme of indole administration has been previously used and found effective in reducing oxidative damage [Sewerynek et al, 1995;Carneiro and Reiter, 1998]. Beginning at the time of ANIT administration and continuing to the end of the study all animals had free access to food and water.…”

Section: Methodsmentioning

confidence: 99%

Characterization of the protective effects of melatonin and related indoles against ?-naphthylisothiocyanate-induced liver injury in rats

et al. 2001

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The protective effect of melatonin, 6-hydroxymelatonin and N-acetylserotonin against alpha-naphthylisothiocyanate (ANIT)-induced liver injury was investigated and compared in rats injected once with the hepatotoxicant (75 mg/kg body weight). In rats injected with ANIT alone, liver injury with cholestasis developed within 24 h, as indicated by both serum levels of alanine aminotransferase (SGPT) and aspartic acid aminotransferase (SGOT) activities and serum total bilirubin concentration. The administration of melatonin or 6-hydroxymelatonin (10 mg/kg body weight) to ANIT-injected rats reduced significantly the serum levels of both SGPT and SGOT and the serum total bilirubin concentration. For all hepatic biochemical markers, melatonin was more effective that 6-hydroxymelatonin. By comparison, the administration of N-acetylserotonin (10 mg/kg body weight) to ANIT-injected rats did not reduce the serum levels of either hepatic enzymes or the serum total bilirubin concentration. In ANIT-injected rats, hepatic lipid peroxidation (LPO) was significantly higher than in control animals and this increase was significantly reduced by either melatonin, 6-hydroxymelatonin or N-acetylserotonin. Furthermore, ANIT treatment caused a significant reduction in liver microsomal membrane fluidity and this reduction was completely reversed by the three indoles. The liver from ANIT-injected rats showed several histopathological alterations; above all there was an acute infiltration of polymorphonuclear neutrophils and an increase in the number of apparent apoptotic hepatocytes. The concurrent administration of melatonin reduced the severity of all morphological alterations, specially the neutrophil infiltration and the number of presumed apoptotic cells. On the contrary, the administration of 6-hydroxymelatonin or N-acetylserotonin did not provide any protective effect in terms of the histopathological alterations. These results indicate that melatonin protects against ANIT-induced liver injury with cholestasis in rats, and suggests that this protective effect is likely due to its antioxidant properties and above all to its capacity to inhibit liver neutrophil infiltration, a critical factor in the pathogenesis of ANIT-induced liver injury. 6-hydroxymelatonin, although able to provide partial protection against the ANIT-induced hepatic injury, probably through its antioxidant properties by mechanisms that are unclear, was unable to reduce neutrophil infiltration. Finally, N-acetylserotonin in the experimental conditions of this study, only exhibited some antioxidant protection but had no protective effect against ANIT-induced hepatic damage.

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“…HIV-1 protease-induced apoptotic cell death was prevented by kynostatin (KNI-272, a selective protease inhibitor) I17] and endogenous antioxidants such as 1713-estradiol [11,42], melatonin [5], and S-nitrosoglutathione [29]. After replicating these findings in vivo, centrally active protease inhibitors and antioxidants can be developed and used for retarding protease-induced progressive cerebral atrophy and associated neuropsychiatric syndrome and dementia complex.…”

Section: Introductionmentioning

confidence: 99%

Kynostatin and 17β-estradiol prevent the apoptotic death of human neuroblastoma cells exposed to HIV-1 protease

1999

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A significant number of adult male patients with acquired immunodeficiency syndrome develop cerebral atrophy and progressive brain disorders such as dementia complex and neuropsychiatric problems. Upon entering the brain via activated macrophages or microglias, the human immunodeficiency type 1 virus (HIV-1) may produce cytotoxic factors such as HIV-1 envelope protein (gp120) and protease. Owing to significant proteolysis of nonviral proteins, the protease derived from HIV-1 may be detrimental to brain cells and neurons. Our results revealed that HIV-1 protease, at nanomolar concentrations, was as potent as gp120 in causing neurotoxicity in human neuroblastoma neurotypic SH-SY5Y cells. As shown by the Oncor ApopTag staining procedure, HIV-1 protease significantly increased the number of apoptotic cells over the serum-free controls. Moreover, HIV-1 protease-induced neurotoxicity was blocked by a selective protease inhibitor, kynostatin (KNI-272). Antioxidants such as 17beta-estradiol, melatonin, and S-nitrosoglutathione also prevented protease-induced neurotoxicity. These findings indicate that oxidative proteolysis may mediate HIV-1 protease-induced apoptosis and the degeneration of neurons and other brain cells. Centrally active protease inhibitors and antioxidants may play an important role in preventing cerebral atrophy and associated dementia complex caused by HIV-1.

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Melatonin protects against lipid peroxidation induced by δ-aminolevulinic acid in rat cerebellum, cortex and hippocampus

Cited by 60 publications

References 41 publications

Aging affects oxidative state in hippocampus, hypothalamus and adrenal glands of Wistar rats

Aging affects oxidative state in hippocampus, hypothalamus and adrenal glands of Wistar rats

Characterization of the protective effects of melatonin and related indoles against ?-naphthylisothiocyanate-induced liver injury in rats

Kynostatin and 17β-estradiol prevent the apoptotic death of human neuroblastoma cells exposed to HIV-1 protease

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