Effect of melatonin on hyperlipidemic nephropathy under constant light exposure

Túnez, Isaac; Muñoz, M. C.; Feijoo-López, M.; Valdelvira, E.; Bujalance-Arenas, I.; Montilla, Pedro

doi:10.1007/bf03179846

Cited by 17 publications

(14 citation statements)

References 12 publications

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“…The renal dysfunction induced by this aminoglycoside was demonstrated by intense proteinuria and high blood urea nitrogen and creatinine concentration in plasma (table 4). These results are in accordance with other studies in which the nephropathies induced by different agents are related to oxidative stress (Guidet & Shan 1989;Yang et al 1995;Montilla et al 1997Montilla et al & 2000Montilla-Ló pez et al 1998;Walker et al 1999;Tú nez et al 2002Tú nez et al & 2003b. Additionally, these data are indirectly in agreement with studies which show that administration of antioxidants reduces nephrotoxicity induced by different agents (Ademuyiwa et al 1990;Ali & Bashir 1996;Erdem et al 2000;Kumar et al 2000;Ozbek et al 2000;Pedraza-Chaverri et al 2000;Maldonado et al 2003;Pedraza-Chaverri et al 2004).…”

Section: Discussionsupporting

confidence: 92%

“…Different studies have shown that melatonin, an indoleamine, has neuro-and nephroprotective effects against experimental-induced oxidative stress in brain and kidney (Montilla-Ló pez et al 1998Benítez-King et al 2003;Montilla et al 2003;Tú nez et al 2002Tú nez et al , 2003a Moreover, the 5HT-depleting agent parachlorophenylalanine (PCPA) is frequently used to evaluate the role of the central serotoninergic system in the regulation of a number of physiological functions, including the secretion of renin by the kidney (Ikonomov et al 1990), the expression of inducible nitric oxide synthase (iNOS), neuronal NOS (nNOS) and nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) in brain (Ramos et al 2002). Furthermore, different reports suggest that serotonin (5HT) may have a relevant antioxidant activity (Ikonomov et al 1990;Liu & Mori 1993;Chan & Tang 1996;Daniels et al 1996;Matuszak et al 1997;Park et al 2002;Ramos et al 2002).…”

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confidence: 99%

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Parachlorophenylalanine Exacerbates Oxidative Stress Induced by Gentamicin in Rats

Muñoz‐Castañeda

Montilla

Muñoz

et al. 2005

Basic Clin Pharma Tox

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The present work studies the effect of parachlorophenylalanine (PCPA, 200 mg/kg intraperitoneally/48 hr for 7 days) on the oxidative stress and nephropathy induced by gentamicin (80 mg/kg intraperitoneally/daily for 7 days) in Wistar rats. The effect of PCPA on lipid peroxidation products and reduced glutathione content in renal and brain tissue, as well as on 5HT content in brain was assessed. Catalase and superoxide dismutase activities were determined in brain tissue. Blood urea nitrogen and creatinine in plasma and total protein content in urine were also measured. Gentamicin caused significant increases in proteinuria, non-protein nitrogen compounds and lipid peroxidation markers, together with decreases in both reduced glutathione content in renal and brain tissue and enzymatic activities in brain homogenates. PCPA harnessed the effect of gentamicin in the brain and the kidney, while PCPA alone induced brain oxidative stress. These results support the prooxidant action of PCPA in brain tissue and its capacity to exacerbate the oxidative stress and renal dysfunction induced by gentamicin, as well as the possible antioxidant property of serotonin.

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Section: Discussionsupporting

confidence: 92%

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confidence: 99%

Parachlorophenylalanine Exacerbates Oxidative Stress Induced by Gentamicin in Rats

Muñoz‐Castañeda

Montilla

Muñoz

et al. 2005

Basic Clin Pharma Tox

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“…In our study, these symptoms appeared to be affected by the photoperiod, which improved some of them in the darkness phase (AD+D vs AD), and made them worse in the permanent light phase (AD+L vs AD). Túnez et al [41] demonstrated that AD and constant light increased the triglyceride and cholesterol levels. These alterations were reverted toward normality by MEL administration, and this would seem to coincide with our results in which the darkness period with higher MEL values appears to improve the pathological symptoms of the AD-induced hyperlipidemic nephropathy.…”

Section: Discussionmentioning

confidence: 99%

Impact of Light/Dark Cycle Patterns on Oxidative Stress in an Adriamycin-Induced Nephropathy Model in Rats

et al. 2014

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The principal goal of this study was to determine the effect of the photoperiod on oxidative damage biomarkers in rats submitted to different light/darkness patterns, in a hyperlipidemic nephropathy model (induced by adriamycin), as well as its possible relationship with melatonin and leptin secretion rhythms. To test this hypothesis, six different groups were used (N = 6 rats per group): control (12 h/12h light:dark); exposure to permanent illumination (24 h light); exposure to darkness (22 h dark); injected with adriamycin, 12h/12h light:dark; injected with adriamycin + exposure to permanent illumination and injected with adriamycin + exposure to darkness (22 h dark). The different photoperiods were begun two weeks prior to medication and were maintained up to the day of the animal's sacrifice, ten days after medication. The following parameters were analysed: i) weight evolution; ii) in plasma: urea, creatinine, uric acid, total proteins, albumen, lactate dehydrogenase, creatinine-quinase, aspartate aminotransferase, alanine aminotransferase and total cholesterol; iii) in urine: urea, creatinine, total proteins and microalbumen; iv) biomarkers of oxidative damage in kidneys, heart, liver and brain: lipoperoxides, total glutathione, reduced glutathione, catalase, glutathione peroxidase, glutathione reductase and glutathione transferase; v) melatonin (pineal gland tissue and plasma) and leptin (plasma). From the results obtained it was concluded that the administration of adriamycin generated oxidative stress in renal, cerebral, hepatic and cardiac tissue. Additionally, in the healthy animal, but of a lesser relevance in the adriamycin animal, permanent light worsened the oxidative stress, whereas darkness improved it. This could be related to the circadian rhythm of the inverse release shown by melatonin and leptin, accentuating the release of melatonin in the darkness phase and that of leptin in the light phase. The correlation between melatonin and leptin in the healthy animal seemed to confirm the relationship between both variables and their influence on oxidative damage biomarkers.

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“…CETP decreased in some acute exercise studies [31], while LCAT increased acutely [32], and as it was mentioned above, melatonin may also increase the activity of this enzyme [30], which would lead to a decrease in the circulating cholesterol and may explain why total cholesterol decreases markedly with melatonin after intense physical exercise. The decrease in the plasma phospholipids levels underlines a significant antihyperlipidemic action of melatonin [33] which could be exerted also by increasing the clearance of endogenous cholesterol [34].…”

Section: Resultsmentioning

confidence: 99%

Melatonin supplementation ameliorates oxidative stress and inflammatory signaling induced by strenuous exercise in adult human males

Ochoa

Díaz-Castro

Kajarabille

et al. 2011

Journal of Pineal Research

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Strenuous exercise induces inflammatory reactions together with high production of free radicals and subsequent muscle damage. This study was designed to investigate for the first time and simultaneously whether over-expression of inflammatory mediators, oxidative stress, and alterations in biochemical parameters induced by acute exercise could be prevented by melatonin. This indoleamine is a potent, endogenously produced free radical scavenger and a broad-spectrum antioxidant; consequently, it might have positive effects on the recovery following an exercise session. The participants were classified into two groups: melatonin-treated men (MG) and placebo-treated individuals (controls group, CG). The physical test consisted in a constant run that combined several degrees of high effort (mountain run and ultra-endurance). The total distance of the run was 50 km with almost 2800 m of ramp in permanent climbing and very changeable climatic conditions. Exercise was associated with a significant increase in TNF-α, IL-6, IL-1ra (in blood), and also an increase in 8-hydroxy-2'-deoxyguanosine (8-OHdG) and isoprostane levels (in urine), and indicated the degree of oxidative stress and inflammation induced. Oral supplementation of melatonin during high-intensity exercise proved efficient in reducing the degree of oxidative stress (lower levels of lipid peroxidation, with a significant increase in antioxidative enzyme activities); this would lead to the maintenance of the cellular integrity and reduce secondary tissue damage. Data obtained also indicate that melatonin has potent protective effects, by preventing over-expression of pro-inflammatory mediators and inhibiting the effects of several pro-inflammatory cytokines. In summary, melatonin supplementation before strenuous exercise reduced muscle damage through modulation of oxidative stress and inflammation signaling associated with this physical challenge.

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Effect of melatonin on hyperlipidemic nephropathy under constant light exposure

Cited by 17 publications

References 12 publications

Parachlorophenylalanine Exacerbates Oxidative Stress Induced by Gentamicin in Rats

Parachlorophenylalanine Exacerbates Oxidative Stress Induced by Gentamicin in Rats

Impact of Light/Dark Cycle Patterns on Oxidative Stress in an Adriamycin-Induced Nephropathy Model in Rats

Melatonin supplementation ameliorates oxidative stress and inflammatory signaling induced by strenuous exercise in adult human males

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