Effect of melatonin on the relationship between lipid peroxidation and proteolytic activity in basal nuclei of rat brain during acute hypoxia

Sopova, I. Yu.; Zamorskii, I. I.

doi:10.1007/s10517-006-0298-6

Cited by 2 publications

(2 citation statements)

References 3 publications

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“…This is in consistent with our previous studies showing the protective effect of melatonin against CIH-induced neuronal and cardiac injuries [7,8]. The known neuroprotective effect of melatonin is, in part, attributed to its antioxidant property against the lipid peroxidation in the central nervous system during oxidative insults [49,50,51]. In fact, melatonin, which directly scavenges ROS, also reduces lipid peroxidation indirectly through mediating an up-regulation of the expression of antioxidant enzymes [52,53].…”

Section: Discussionsupporting

confidence: 92%

Melatonin Attenuates Intermittent Hypoxia-Induced Lipid Peroxidation and Local Inflammation in Rat Adrenal Medulla

Liu

Tipoe

Fung

2014

IJMS

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Chronic intermittent hypoxia (CIH) induces lipid peroxidation and leads to cardiovascular dysfunction, in which impaired activities of the adrenal medulla are involved. This may be caused by CIH-induced injury in the adrenal medulla, for which the mechanism is currently undefined. We tested the hypothesis that melatonin ameliorates the CIH-induced lipid peroxidation, local inflammation and cellular injury in rat adrenal medulla. Adult Sprague–Dawley rats were exposed to air (normoxic control) or hypoxia mimicking a severe recurrent sleep apnoeic condition for 14 days. The injection of melatonin (10 mg/kg) or vehicle was given before the daily hypoxic treatment. We found that levels of malondialdehyde and nitrotyrosine were significantly increased in the vehicle-treated hypoxic group, when compared with the normoxic control or hypoxic group treated with melatonin. Also, the protein levels of antioxidant enzymes (superoxide dismutase (SOD)-1 and SOD-2) were significantly lowered in the hypoxic group treated with vehicle but not in the melatonin group. In addition, the level of macrophage infiltration and the expression of inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6) and mediators (inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2)) were elevated in the vehicle-treated hypoxic group, but were significantly ameliorated by the melatonin treatment. Moreover, the amount of apoptotic cells in the hypoxic groups was significantly less in the melatonin-treated group. In conclusion, CIH-induced lipid peroxidation causes local inflammation and cellular injury in the adrenal medulla. The antioxidant and anti-inflammatory actions of melatonin are indicative of a protective agent against adrenal damage in patients with severe obstructive sleep apnea syndrome.

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Section: Discussionsupporting

confidence: 92%

Melatonin Attenuates Intermittent Hypoxia-Induced Lipid Peroxidation and Local Inflammation in Rat Adrenal Medulla

Liu

Tipoe

Fung

2014

IJMS

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“…In fact, lipid peroxidation is one of the major processes mediating the breakdown of membrane lipids leading to neuronal injury [40, 41]. It has been suggested that the neuroprotective effect of melatonin could be attributed to the antioxidant property, which prevents the lipid peroxidation in the central nervous system during oxidative insults [42–44]. This is supported by results of this study and also by our recent observation that melatonin mitigates IH‐induced oxidative stress and prevents inflammation and apoptosis in the hippocampus [30].…”

Section: Discussionmentioning

confidence: 99%

Melatonin ameliorates hippocampal nitric oxide production and large conductance calcium‐activated potassium channel activity in chronic intermittent hypoxia

Tjong¹,

Li²,

Hung³

et al. 2007

Journal of Pineal Research

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Melatonin protects against hippocampal injury induced by intermittent hypoxia (IH). IH-induced oxidative stress is associated with decreases in constitutive production of nitric oxide (NO) and in the activity of large conductance calcium-activated potassium (BK) channels in hippocampal neurons. We tested the hypothesis that administration of melatonin alleviates the NO deficit and impaired BK channel activity in the hippocampus of IH rats. Sprague-Dawley rats were injected with melatonin (10 mg/kg, i.p.) or vehicle before daily IH exposure for 8 hr for 7 days. The NO and intracellular calcium ([Ca2+]i) levels in the CA1 region of hippocampal slices were measured by electrochemical microsenor and spectrofluorometry, respectively. The activity of BK channels was recorded by patch-clamping electrophysiology in dissociated CA1 neurons. Malondialdehyde levels were increased in the hippocampus of hypoxic rats and were lowered by the melatonin treatment. Levels of NO under resting and hypoxic conditions, and the protein expression of neuronal NO synthase (nNOS) were significantly reduced in the CA1 neurons of hypoxic animals compared with the normoxic controls. These deficits were mitigated in the melatonin-treated hypoxic rats with an improved [Ca2+]i response to acute hypoxia. The open probability of BK channels was decreased in the hypoxic rats and was partially restored in the melatonin-treated animals, without alterations in the expression of channel subunits and unitary conductance. Acute treatment of melatonin had no significant effects on the BK channel activity or on the [Ca2+]i response to hypoxia. Collectively, these results suggest that melatonin ameliorates the constitutive NO production and BK channel activity via an antioxidant mechanism against an IH-induced down-regulation of nNOS expression in hippocampal neurons.

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Effect of melatonin on the relationship between lipid peroxidation and proteolytic activity in basal nuclei of rat brain during acute hypoxia

Cited by 2 publications

References 3 publications

Melatonin Attenuates Intermittent Hypoxia-Induced Lipid Peroxidation and Local Inflammation in Rat Adrenal Medulla

Melatonin Attenuates Intermittent Hypoxia-Induced Lipid Peroxidation and Local Inflammation in Rat Adrenal Medulla

Melatonin ameliorates hippocampal nitric oxide production and large conductance calcium‐activated potassium channel activity in chronic intermittent hypoxia

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