The influence of brain acetaldehyde on oxidative status, dopamine metabolism and visual discrimination task

Heap, Laura C.; Ward, Roberta J.; Abiaka, Clifford; Dexter, David T.; Lawlor, Monica; Pratt, O. E.; Thomson, Allan D.; Shaw, Ken; Peters, Timothy J.

doi:10.1016/0006-2952(94)00539-x

Cited by 59 publications

(32 citation statements)

References 39 publications

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“…Although it has been suggested that acetaldehyde does not readily cross the blood-brain barrier (Seeman et al, 2002), in the absence of studies of CNS penetration during early adolescence, it is premature to conclude that acetaldehyde does not enter the brain of juvenile animals. Substantial penetration of acetaldehyde into adult brain has been observed following a single intraperitoneal (Heap et al, 1995) or intravenous (Foddai et al, 2004) injection, but at doses considerably higher than those used here. Acetaldehyde has also been shown to display rewarding effects when injected either peripherally (Quintanilla and Tampier, 2003a) or directly into the posterior ventral tegmental area (Rodd-Henricks et al, 2002), but again at doses higher than those used here.…”

Section: Mechanistic Considerationsmentioning

confidence: 55%

Acetaldehyde Enhances Acquisition of Nicotine Self-Administration in Adolescent Rats

Belluzzi

Wang

Leslie

2004

Neuropsychopharmacol

220

213

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Tobacco use has one of the highest rates of addiction and relapse of any abused drug. Paradoxically, however, in animal models of reinforcement nicotine appears weak compared to other abused drugs. We report here that acetaldehyde, a major component of tobacco smoke, enhances nicotine self-administration. Juvenile and adult male rats were implanted with intravenous catheters and tested for self-administration 4 days later at postnatal day 27 or 90, respectively. Animals were tested, without prior response training, in five daily 3-h sessions where each nose-poke delivered an intravenous injection followed by a 60-s timeout. Animals (11-13/group) were offered one of the following solutions: nicotine (30 mg/kg/injection), acetaldehyde (16 mg/kg/inj), nicotine (30 mg/kg/inj) þ acetaldehyde (16 mg/kg/inj), or saline. The youngest animals responded significantly more for nic þ acet than for saline or for either drug alone. Responding at the reinforced hole was significantly higher than at the nonreinforced hole or at the reinforced hole during noncontingent injections of nic þ acet. Tests with receptor antagonists indicated that these drug effects are mediated by central, but not peripheral, nicotinic receptors. There was an age-related decline in self-administration of nic þ acet, but not for cocaine. Taken together, these results indicate that acetaldehyde, at the low concentrations found in tobacco smoke, interacts with nicotine to increase responding in a stringent self-administration acquisition test where nicotine alone is only weakly reinforcing, and that adolescent animals are more sensitive to these actions than adults. Animal models of tobacco addiction could be improved by combining acetaldehyde, and possibly other smoke components, with nicotine to more accurately reflect the pharmacological profile of tobacco smoke.

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Section: Mechanistic Considerationsmentioning

confidence: 55%

Acetaldehyde Enhances Acquisition of Nicotine Self-Administration in Adolescent Rats

Belluzzi

Wang

Leslie

2004

Neuropsychopharmacol

220

213

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“…In the present study, the graded ethanol exposure augmented the catalase activities in different ethanol groups in a dose-dependent manner ( Table 2). Similar enhanced catalase activities in brain due to ethanol had been demonstrated in animal studies [44] as well as cell cultures studies [45]. However, the augmentations in brain catalase activities have been trimmed down by the coexposure of aluminum (Table 2).…”

Section: Discussionmentioning

confidence: 63%

Augmentation of Aluminum-Induced Oxidative Stress in Rat Cerebrum by Presence of Pro-oxidant (Graded Doses of Ethanol) Exposure

2010

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Both aluminum and ethanol are pro-oxidants and neurotoxic. Considering the possibilities of co-exposure and sharing mechanisms of producing neurotoxicity, the present study was planned to identify the level of aluminum-induced oxidative stress in altered pro-oxidant (ethanol exposure) status of cerebrum. Male rats were coexposed to aluminum and ethanol for 4 weeks. After the exposure period, cerebral levels of protein, reduced glutathione (GSH), lipid peroxidation (TBARS) were measured. Activities of catalase, superoxide dismutase (SOD), glutathione reductase (GR) and glutathione perioxidase (GPx) of cerebrum were estimated. In most of the cases significant correlations were observed between the alterations and graded ethanol doses, suggesting a dose-dependency in pushing the oxidant equilibrium toward pro-oxidants. Aluminum is found to influence significantly all the studied parameters of oxidative stress. Likewise, ethanol also influenced these parameters significantly, except GR, while the interaction between ethanol and aluminum could significantly influence only the GSH content and GR activity of cerebrum. Present study demonstrate that coexposure of aluminum with pro-oxidant might favor development of aluminum-induced oxidative stress in cerebrum. This observation might be helpful in understanding of mechanism of neurodegenerative disorders and ameliorate them.

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“…Therefore, the 560 mg/kg acetaldehyde dose was withdrawn from the present study. In previous studies, the IP injection of acetaldehyde in doses such as those used in the present experiment, was shown to result in a rapid increase in brain acetaldehyde content together with significant behavioral effects (Heap et al 1995;Ward et al 1997;Quertemont and De Witte 2001;Quertemont and Grant 2002).…”

Section: Methodsmentioning

confidence: 91%

“…Such a concentration is more than 10 times higher than the concentrations typically found after the administration of 1.0 g/kg ethanol to cyanamide-pretreated rats and far exceeds the blood concentrations required for acetaldehyde to saturate the brain microvasculature ALDH and to cross the blood-brain barrier. Indeed, very significant brain acetaldehyde concentrations were measured in the brain after the IP administration of 20-100 mg/kg acetaldehyde (Heap et al 1995;Ward et al 1997). Quertemont and De Witte (2001) recently showed place preferences after conditioning with such IP doses of acetaldehyde, suggesting that the strong positively reinforcing effects of brain acetaldehyde that crossed the blood brain barrier overshadowed the aversive effects of peripheral acetaldehyde accumulation.…”

Section: Discussionmentioning

confidence: 98%

Role of acetaldehyde in ethanol-induced conditioned taste aversion in rats

2003

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The influence of brain acetaldehyde on oxidative status, dopamine metabolism and visual discrimination task

Cited by 59 publications

References 39 publications

Acetaldehyde Enhances Acquisition of Nicotine Self-Administration in Adolescent Rats

Acetaldehyde Enhances Acquisition of Nicotine Self-Administration in Adolescent Rats

Augmentation of Aluminum-Induced Oxidative Stress in Rat Cerebrum by Presence of Pro-oxidant (Graded Doses of Ethanol) Exposure

Role of acetaldehyde in ethanol-induced conditioned taste aversion in rats

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