Effects of curcumin and tannic acid on the aluminum- and lead-induced oxidative neurotoxicity and alterations in NMDA receptors

Tüzmen, Nalan; Yücel, Nilgün Candan; Kalburcu, Tülden; Demiryas, Nazan

doi:10.3109/15376516.2014.997947

Cited by 43 publications

(21 citation statements)

References 49 publications

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“…Previous studies have reported that curcumin decreases AChE activity in rat brain [51][52][53]. In vitro experiments also confirmed that curcumin inhibits AChE activity and has an IC 50 value of 67 µmol/L [54].…”

Section: Discussionsupporting

confidence: 61%

Inhibition of Nicotine Dependence by Curcuminoid Is Associated with Reduced Acetylcholinesterase Activity in the Mouse Brain

et al. 2018

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Nicotine is a stimulatory component in tobacco that activates the central nervous system reward pathway and causes nicotine dependence. We found that the anti-inflammatory agent, curcuminoid, prevents nicotine dependence and relapse, as assessed by the conditioned placed preference test. Curcuminoid (1, 3.2, and 10 mg·kg^–1, oral) dose-dependently inhibited nicotine dependence and enhanced nicotine extinction when administrated 30 min prior to nicotine administration (0.5 mg·kg^–1, i.p.) for 7 days. In addition, curcuminoid significantly suppressed the priming effects of nicotine and inhibited acetylcholinesterase (AChE) activity. Taken together, curcuminoid ameliorates nicotine dependence and relapse, in part via the inhibition of the AChE activity in the brain.

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Section: Discussionsupporting

confidence: 61%

Inhibition of Nicotine Dependence by Curcuminoid Is Associated with Reduced Acetylcholinesterase Activity in the Mouse Brain

et al. 2018

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“…Tu Baijie's study found that BaP and lead exert synergistic effects; BaP can enhance the neurotoxicity of lead (Tu et al, 2004). Both aluminum and lead are neurotoxic metals and are thought to be related to neurodegenerative dis-eases (Weidenhamer et al, 2014); their toxicity mechanisms are similar (Tüzmen et al, 2014). According to the present study, BaP may enhance the neurotoxicity of aluminum, which warrants further study.…”

Section: Discussionmentioning

confidence: 58%

Aluminum and benzo[a]pyrene co-operate to induce neuronal apoptosis <i>in vitro </i>

et al. 2015

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Toxic and harmful factors co-exist in the environment; these factors often interact to induce combined toxicity, which is the main focus of toxicological research. Furthermore, a large number of studies have shown that aluminum (Al) and benzo[a]pyrene (BaP) are neurotoxic and target the central nervous system to cause neuronal apoptosis. Because we are exposed to both Al and BaP in the air, water, food, and even medicine, the combined effects of these agents in humans must be examined. The present study examines the ability of Al and BaP co-exposure to intensify neuronal apoptosis. The primary neurons of newborn rats were cultured for 5 days, and cells from the same batch that were growing well were selected and assigned to the blank control group, the solvent control group (DMSO+S9+maltol), BaP groups (10, 40 μmol/L), Al (mal)3 groups (50, 100, 400 μmol/L) and co-exposure groups with different combinations of BaP and Al (mal)3. The cell viabilities indicated that 10 μM BaP or 50 μM Al (mal)3 was mildly toxic, and we selected 10 μM BaP+50 μM Al (mal)3 for subsequent co-exposure experiments. The morphological characteristics of cell apoptosis were much more obvious in the co-exposure group than in the Al-exposed cells or the BaP-exposed cells, as observed with a transmission electron microscope and a fluorescence inverted microscope. The apoptotic rates and caspase-3 activity quantitatively significantly differed between the co-exposure and Al-exposure groups, while the BaP-exposure group did not significantly differ from the control group. These results indicate that Al and BaP co-exposure exert synergistic effects on neuronal cell apoptosis.

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“…increase of the concentrations of NR2A and NR2B subunits of N -methyl- d -aspartate receptors, elevation of the activities of antioxidant enzymes, decrease of lipid peroxidation in the brain hippocampus in Wistar rats after 16-weeks exposure of animals to Al 3+ and Pb 2+ (tannic acid at 50 mg/kg b.w./day; a nasogastric probe was used) [91];…”

Section: Figurementioning

confidence: 99%

The Neuroprotective Effects of Phenolic Acids: Molecular Mechanism of Action

2017

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The neuroprotective role of phenolic acids from food has previously been reported by many authors. In this review, the role of phenolic acids in ameliorating depression, ischemia/reperfusion injury, neuroinflammation, apoptosis, glutamate-induced toxicity, epilepsy, imbalance after traumatic brain injury, hyperinsulinemia-induced memory impairment, hearing and vision disturbances, Parkinson’s disease, Huntington’s disease, anti-amyotrophic lateral sclerosis, Chagas disease and other less distributed diseases is discussed. This review covers the in vitro, ex vivo and in vivo studies concerning the prevention and treatment of neurological disorders (on the biochemical and gene expression levels) by phenolic acids.

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Effects of curcumin and tannic acid on the aluminum- and lead-induced oxidative neurotoxicity and alterations in NMDA receptors

Cited by 43 publications

References 49 publications

Inhibition of Nicotine Dependence by Curcuminoid Is Associated with Reduced Acetylcholinesterase Activity in the Mouse Brain

Inhibition of Nicotine Dependence by Curcuminoid Is Associated with Reduced Acetylcholinesterase Activity in the Mouse Brain

Aluminum and benzo[a]pyrene co-operate to induce neuronal apoptosis <i>in vitro </i>

The Neuroprotective Effects of Phenolic Acids: Molecular Mechanism of Action

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