Developmental lead exposure induces opposite effects on ethanol intake and locomotion in response to central vs. systemic cyanamide administration

Mattalloni, Mara Soledad; Deza-Ponzio, Romina; Albrecht, Paula A.; Cancela, Liliana Marina; Virgolini, Miriam Beatríz

doi:10.1016/j.alcohol.2016.11.002

Cited by 12 publications

(14 citation statements)

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“…The square bracket comprises pictures for brain, liver and blood CAT and ALDH2 status and putative acetaldehyde (ACD) accumulation in the experimental model described in Mattalloni et al (2013, 2017; as shown on the left). The references point-out CAT and ALDH2 data reported elsewhere as result of adult acute or chronic Pb exposure in animals with chronic EtOH intake.…”

Section: Resultsmentioning

confidence: 99%

“…Similarly, we have reported that developmental Pb exposure increased basal blood CAT activity in periadolescent rats, an effect that persisted throughout their lifetime and was potentiated by EtOH intake. Although no differences between groups were observed in whole brain CAT activity, there was a region-specific increase in the Pb-exposed hippocampus and cerebellum, indicating that CAT-mediated EtOH oxidation is not homogeneous throughout the brain (Mattalloni et al, 2013, 2017). …”

Section: Lead Ethanol and The Two Faces Of Reinforcementmentioning

confidence: 99%

“…The two evidences of an interaction between Pb and ALDH2 have shown that adult Pb exposure reduced liver ALDH2 (Flora and Tandon, 1987) whereas developmental Pb-exposure reduced brain ALDH2 activity (Mattalloni et al, 2017) after chronic EtOH consumption.…”

Section: Lead Ethanol and The Two Faces Of Reinforcementmentioning

confidence: 99%

“…CY administration: *denotes differences between the C and Pb-exposed animals injected with VEH at *** p < 0.001; # denotes differences between the VEH and corresponding CY groups for both C and Pb-exposed animals at ### p < 0.001. C-VEH = 11; C-CY i.c.v.= 14; Pb-VEH = 8; Pb-CY i.c.v.= 8 animals per group (Mattalloni et al, 2017). …”

Section: Pharmacological Interference Of Ethanol Metabolismmentioning

confidence: 99%

“…We have demonstrated that i.c.v. CY administration inhibited brain ALDH2 and increased EtOH intake in control animals, whereas the Pb-exposed group also showed elevated EtOH intake although in the absence of brain ALDH2 inhibition (Mattalloni et al, 2017). This finding may be related to the reduced basal brain ALDH2 activity present in the Pb-exposed group, or to the fact that CY is a prodrug that, to convert itself to the active metabolite requires CAT and H 2 O 2 , a system that is modified by Pb-exposure.…”

Section: Pharmacological Interference Of Ethanol Metabolismmentioning

confidence: 99%

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Modulation of Ethanol-Metabolizing Enzymes by Developmental Lead Exposure: Effects in Voluntary Ethanol Consumption

Virgolini

Mattalloni

Albrecht

et al. 2017

Front. Behav. Neurosci.

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This review article provides evidence of the impact of the environmental contaminant lead (Pb) on the pattern of the motivational effects of ethanol (EtOH). To find a mechanism that explains this interaction, the focus of this review article is on central EtOH metabolism and the participating enzymes, as key factors in the modulation of brain acetaldehyde (ACD) accumulation and resulting effect on EtOH intake. Catalase (CAT) seems a good candidate for the shared mechanism between Pb and EtOH due to both its antioxidant and its brain EtOH-metabolizing properties. CAT overactivation was reported to increase EtOH consumption, while CAT blockade reduced it, and both scenarios were modified by Pb exposure, probably as the result of elevated brain and blood CAT activity. Likewise, the motivational effects of EtOH were enhanced when brain ACD metabolism was prevented by ALDH2 inhibition, even in the Pb animals that evidenced reduced brain ALDH2 activity after chronic EtOH intake. Overall, these results suggest that brain EtOH metabolizing enzymes are modulated by Pb exposure with resultant central ACD accumulation and a prevalence of the reinforcing effects of the metabolite in brain against the aversive peripheral ACD accumulation. They also support the idea that early exposure to an environmental contaminant, even at low doses, predisposes at a later age to differential reactivity to challenging events, increasing, in this case, vulnerability to acquiring addictive behaviors, including excessive EtOH intake.

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Section: Resultsmentioning

confidence: 99%

Section: Lead Ethanol and The Two Faces Of Reinforcementmentioning

confidence: 99%