Melatonin reduces both basal and bacterial lipopolysaccharide-induced lipid peroxidation in vitro

Sewerynek, Ewa; Melchiorri, Daniela; Chen, Li-Dun; Reíter, Russel J.

doi:10.1016/0891-5849(95)00101-3

Cited by 139 publications

(93 citation statements)

References 36 publications

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“…We observed no significant difference in the activity SOD in the brain tissues between groups. It has been previously shown that LPS disturbs the oxidative status and energy metabolism in the brain 29 . In has also been reported that LPS increases the level of MDA and reduces glutathione (GH) while, does not change the activity of SOD 30 .…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide-induced memory impairment in rats is preventable using 7-nitroindazole

Anaeigoudari

Shafei

Soukhtanloo

et al. 2015

Arq. Neuro-Psiquiatr.

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Inflammation and oxidative stress have important roles in memory impairment. The effect of 7-nitroindazole (7NI) on lipopolysaccharide (LPS)-induced memory impairment was investigated. Rats were used, divided into four groups that were treated as follows: (1) control (saline); (2) LPS; (3) 7NI-LPS; and (4) 7NI before passive avoidance (PA). In the LPS group, the latency for entering the dark compartment was shorter than in the controls (p < 0.01 and p < 0.001); while in the 7NI-LPS group, it was longer than in the LPS group (p < 0.01 and p < 0.001). Malondialdehyde (MDA) and nitric oxide (NO) metabolite concentrations in the brain tissues of the LPS group were higher than in the controls (p < 0.001 and p < 0.05); while in the 7NI-LPS group, they were lower than in the LPS group (p < 0.001 and p < 0.05, respectively). The thiol content in the brain of the LPS group was lower than in the controls (p < 0.001); while in the 7NI-LPS group, it was higher than in the LPS group (p < 0.001). It is suggested that brain tissue oxidative damage and NO elevation have a role in the deleterious effects of LPS on memory retention that are preventable using 7NI.

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Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide-induced memory impairment in rats is preventable using 7-nitroindazole

Anaeigoudari

Shafei

Soukhtanloo

et al. 2015

Arq. Neuro-Psiquiatr.

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“…Beneficial effects of the pineal hormone melatonin on tissue oxidative damage have been demonstrated in studies on experimental models. In these studies, it was shown that melatonin has highly potent free radical scavenging ability and it was suggested that this action may contribute to the antiinflammatory effects of this agent (12,(19)(20)(21)(22)(23). However, this possible mechanism must be supported by measuring antioxidant enzyme activities.…”

Section: Discussionmentioning

confidence: 99%

“…The antioxidant and antiinflammatory effects of the pineal hormone melatonin (17,18) on tissue oxidative damage were well demonstrated in several studies on experimental models (19)(20)(21)(22)(23). Additionally, in our previous study, we showed that melatonin could prevent and restore the contractile impairment of the cavernous tissue in mice treated with bacterial LPS (12).…”

Section: Introductionmentioning

confidence: 99%

Effect of melatonin on contractile activity in intraurethrally instilled E. coli-induced acute prostatitis rat model

Huseynov¹,

Eser²,

Aridogan³

et al. 2013

Turk J Med Sci

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In the present study, some new 2-(pyridin-2-yl)thieno [2,3-d ]pyrimidin-4(3 H)-ones derivatives (IIa-o) were synthesized. The target compounds (IIa-o) were synthesized through the acid catalyzed condensation of 2-cyano, 3-cyano, and 4-cyano-pyridines with various 2-amino-3-carbethoxythiophenes (Ia-e). All thiophene derivatives were synthesized by Gewald reaction. The structures of the newly synthesized compounds were confirmed by UV-Visible, FT-IR, 1 H-NMR, and mass spectral studies. All synthesized compounds were evaluated for their antimicrobial activity against various gram-positive and gram-negative bacterial and fungal strains. Amongst the synthesized compounds IIa, IIb, IId, IIe, and IIm were found to be active.

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“…Some of the most toxic agents which have been utilized and shown to be counteracted by melatonin include the excitatory neurotransmitter analogue kainic acid (71)(72)(73), H202 (74,75), potassium cyanide (76), lipopolysaccharide (60,77,78), hydrophobic bile acids (79), carbon tetrachloride (61), and the carcinogen safrole (63,64). Also, the damage caused by a physical agent, i.e., ionizing radiation (65,80), and a highly destructive experimental procedure known to generate free radicals, i.e., induced ischemia followed by reperfusion (81)(82)(83), has been shown to be reduced by concurrent melatonin administration.…”

Section: Melatonin As An Antioxidantmentioning

confidence: 99%

“…4). It does seem likely that melatonin has beneficial effects in all cells to help them cope with the devastating actions of toxins (60,62,64), to resist viral infections (125,126), and to overcome debilitating changes associated with aging (84,86,116). How effective physiological or pharmacological levels of melatonin will eventually prove to be in terms of protecting against the inevitable and insidious changes of aging is currently being intensely investigated.…”

Section: Final Commentmentioning

confidence: 99%

Aging and oxygen toxicity: Relation to changes in melatonin

Reíter

1997

AGE

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Melatonin (N-acetyl-5-methoxytryptamine) is a chemical mediator produced in the pineal gland and other sites in the body. The melatonin found in the blood is derived almost exclusively from the pineal gland. Since the pineal synthesizes melatonin primarily at night, blood levels of the indole are also higher at night (5-15 fold) than during the day. Some individuals on a nightly basis produce twice as much melatonin as others of the same age. Throughout life, the melatonin rhythm gradually wanes such that, in advanced age, melatonin production is usually at a minimum. Melatonin was recently found to be a free radical scavenger and antioxidant. It has been shown, in the experimental setting, to protect against both free radical induced DNA damage and oxidative stress-mediated lipid peroxidation. Pharmacologically, melatonin has been shown to reduce oxidative damage caused by such toxins as the chemical carcinogen safrole, carbon tetrachloride, paraquat, bacterial lipopolysaccharide, kainic acid, 8-aminolevulinic and amyloid 13 peptide of AIzheimer's disease as well as a model of Parkinson's disease involving the drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Additionally, the oxidative damage caused by agents such as ionizing radiation and excessive exercise is reduced by melatonin. Since free radical-induced molecular injury may play a significant role in aging, melatonin's ability to protect against it suggests a potential function of melatonin in deferring aging and agerelated, free radical-based diseases. Besides its ability to abate oxidative damage, other beneficial features of melatonin may be important in combating the signs of aging; these include melatonin's immune-stimulating function, its sleep-promoting ability, its function as an anti-viral agent, and general protective actions at the cellular level. Definitive tests of the specific functions of physiological levels of melatonin in processes of aging are currently being conducted.

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Melatonin reduces both basal and bacterial lipopolysaccharide-induced lipid peroxidation in vitro

Cited by 139 publications

References 36 publications

Lipopolysaccharide-induced memory impairment in rats is preventable using 7-nitroindazole

Lipopolysaccharide-induced memory impairment in rats is preventable using 7-nitroindazole

Effect of melatonin on contractile activity in intraurethrally instilled E. coli-induced acute prostatitis rat model

Aging and oxygen toxicity: Relation to changes in melatonin

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