Protection of methamphetamine nigrostriatal toxicity by dietary selenium

Kim, Hyoung‐Chun; Jhoo, Wang-Kee; Choi, Dong‐Young; Im, Doo-Hyun; Shin, Eun‐Joo; Suh, Jeong-Hye; Floyd, Robert A.; Bing, Guoying

doi:10.1016/s0006-8993(99)02122-8

Cited by 93 publications

(71 citation statements)

References 53 publications

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“…The present findings support the hypothesis that decreased SOD activity can lead to an accumulation of H 2 O 2 which, in the absence of a simultaneous increase in GPX activity, could increase the Fenton reaction, leading to the stimulation of lipid peroxidation and protein oxidation resulting, in cellular damage [44][45][46]. Also, we observed a significant increase in ROS production in rat temporal cortex which is comparable to other previously reported data [47,48].…”

Section: Discussionsupporting

confidence: 92%

Nicotine-induced memory impairment by increasing brain oxidative stress

Hrițcu

Ciobîcă²,

Gorgan

2009

Open Life Sciences

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Male Wistar rats were subjected to chronic nicotine treatment (0.3 mg/kg; 7 continuous days) and their memory performance was studied by means of Y-maze and multi-trial passive avoidance tasks. Nicotine significantly decreased spontaneous alternation in Y-maze task and step-through-latency in the multi-trial passive avoidance task, suggesting effects on both short-term memory and long-term memory, respectively. In addition, nicotine induced neuronal apoptosis, DNA fragmentation, reduced antioxidant enzymes activity, and increased production of lipid peroxidation and reactive oxygen species, suggesting pro-oxidant activity. Our results provide further support that nicotine-induced memory impairment is due to an increase in brain oxidative stress in rats.

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Section: Discussionsupporting

confidence: 92%

Nicotine-induced memory impairment by increasing brain oxidative stress

Hrițcu

Ciobîcă²,

Gorgan

2009

Open Life Sciences

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“…Brain (occipital cortex) drug levels for the high and low groups are 124 Ϯ 47 (range, 20 -319; median 90) and 10.0 Ϯ 1.3 (range, 2.8 -15.6; median 10) nmol/g tissue, respectively (p Ͻ 0.01, Mann-Whitney U tests). Dopamine levels (previously reported by Wilson et al, 1996 andMoszczynska et al, 2004) Kim et al, 1999;Kita et al, 2000;Wan et al, 2000;Gluck et al, 2001;Flora et al, 2002;Iwashita et al, 2004). Nevertheless, the possibility also has to be considered that chronic drug exposure (e.g., involving tolerance, sensitization) might also have modulated the effects of an acute exposure, as suggested by some animal data (Acikgoz et al, 1998(Acikgoz et al, , 2000.…”

Section: Discussionmentioning

confidence: 90%

“…We hypothesized that, as in most of the experimental animal studies in which MDA or MDA-like thiobarbituric acid reactive substances (TBARS) were reported to be increased in brain of MA-treated rodents (Acikgoz et al, 1998(Acikgoz et al, , 2000Jayanthi et al, 1998;Yamamoto and Zhu, 1998;Kim et al, 1999;Kita et al, 2000;Wan et al, 2000;Gluck et al, 2001;Flora et al, 2002;Iwashita et al, 2004), levels of both oxidative markers would be above-normal in the dopamine-rich caudate nucleus of human MA users but less markedly increased (if at all) in brain areas having very low (frontal and cerebellar cortices) concentrations of dopamine. Our human post mortem data provide additional support to the notion based on animal models that MA can cause oxidative damage in human brain.…”

mentioning

confidence: 99%

Levels of 4-Hydroxynonenal and Malondialdehyde Are Increased in Brain of Human Chronic Users of Methamphetamine

Fitzmaurice

Tong²,

Yazdanpanah³

et al. 2006

J Pharmacol Exp Ther

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Animal studies suggest that the widely used psychostimulant drug methamphetamine (MA) can harm brain dopamine neurones, possibly by causing oxidative damage. However, evidence of oxidative damage in brain of human MA users is lacking. We tested the hypothesis that levels of two "gold standard" products generated from lipid peroxidation, 4-hydroxynonenal (one of the most reactive lipid peroxidation aldehyde products) and malondialdehyde, would be elevated in post mortem brain of 16 dopamine-deficient chronic MA users compared with those in 21 matched control subjects. Derivatized aldehyde concentrations were determined by gas chromatography-mass spectrometry. In the MA group, we found significantly increased levels of 4-hydroxynonenal and malondialdehyde in the dopamine-rich caudate nucleus (by 67 and 75%, respectively) and to a lesser extent in frontal cortex (48 and 36%, respectively) but not in the cerebellar cortex. Approximately half of the MA users had levels of 4-hydroxynonenal falling above the upper limit of the control range in caudate and frontal cortex. A subgroup of MA users with high brain drug levels had higher concentrations of the aldehydes. Our data suggest that MA exposure in human causes, as in experimental animals, above-normal formation of potentially toxic lipid peroxidation products in brain. This provides evidence for involvement of oxygen-based free radicals in the action of MA in both dopamine-rich (caudate) and -poor (cerebral cortex) areas of human brain.

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“…The amount of lipid peroxidation was determined by measuring the accumulation of thiobarbituric acid-reactive substances in homogenates of hippocampal tissue and is expressed as MDA content (Jareno et al, 1998;Kim et al, 1999bKim et al, , 2000cKim et al, , 2002a. In brief, 0.1 ml of the homogenate (or standard solutions prepared daily from 1,1,3,3-tetra-methoxypropane) and 0.75 ml of the working solution (thiobarbituric acid 0.37% and perchloric acid 6.4%, 2:1 v/v) were mixed and heated to 95°C for 1 h. After cooling (10 min in ice water bath), the flocculent precipitate was removed by centrifugation at 3200ϫg for 10 min.…”

Section: Determination Of Mdamentioning

confidence: 99%

“…GSH and GSSG were immediately measured from dissected hippocampal tissues by the method described by Reed et al (1980) with minor modification (Kim et al, 1999b(Kim et al, , 2000c. Briefly, a sample of the acidified supernatant was added to the internal standard (1 mM cysteic acid) and 0.88 M iodoacetic acid.…”

Section: Determination Of Gsh and Gssgmentioning

confidence: 99%