[d-Pen2,d-Pen5]Enkephalin, a δ opioid agonist, reduces endogenous aluminum content in the rat central nervous system

Gulya, Károly; Szikra, Judit; Kása, P.

doi:10.1016/0306-4522(94)00575-p

Cited by 5 publications

(2 citation statements)

References 41 publications

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“…It has been shown that Al 3+ binds at two metal-binding sites of enkephalin, involving the Tyr1CO and Leu5COO À groups of the neuropeptide in dimethyl sulphoxide solution [130]. Moreover, [D-Pen 2 ,D-Pen 5 ]enkephalin, when intraventricularly injected, transiently reduces the aluminium content of striatum and parietal cortex in chronically exposed rats to AlCl 3 [131]. Rao et al [132] showed that neuropeptide Y complexes with aluminium, altering its biological activity.…”

Section: Neurotransmitter Synthesis and Storagementioning

confidence: 98%

“…Interestingly, the 5-hydroxytryptamine receptors class 2 couple preferentially to G q /G 11 to increase the hydrolysis of inositol phosphates and elevate cytosolic Ca 2+ concentrations. Chronic systemic in vivo, as well as in vitro, effects of aluminium on opioid receptor binding characteristics were also studied [131]. Neither the specific agonist binding to d nor to l opioid receptors was modified.…”

Section: Neurotransmitter Interaction With Receptorsmentioning

confidence: 99%

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Does neurotransmission impairment accompany aluminium neurotoxicity?

Gonçalves

Silva

2007

Journal of Inorganic Biochemistry

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Section: Neurotransmitter Synthesis and Storagementioning

confidence: 98%

Section: Neurotransmitter Interaction With Receptorsmentioning

confidence: 99%

Does neurotransmission impairment accompany aluminium neurotoxicity?

Gonçalves

Silva

2007

Journal of Inorganic Biochemistry

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The Role of δ-Opioid Receptors in Brain Ionic Homeostasis Under Physiological Condition

Chao¹,

Xia²

2015

Neural Functions of the Delta-Opioid Receptor

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Aluminum but not iron treatment induces pro-oxidant events in the rat brain

Bondy

Ali

Guo‐Ross

1998

Molecular and Chemical Neuropathology

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In an attempt to delineate the capacity of aluminum (Al) to promote pro-oxidant events, several indices of oxidative stress have been determined in brains and livers of rats exposed to an Al salt, either alone or in combination with an iron (Fe) compound. Treatment with Al over a 3-wk period increased both cortical levels of glutathione (GSH) and the rates of generation of reactive oxygen species (ROS). Dosing with an Fe compound resulted in no parallel changes, and concurrent exposure to Fe together with Al prevented these elevations. Both Fe and Al dosing elevated glutamine synthetase activity in the cortex. Levels of creatine kinase, another enzyme susceptible to oxidative stress, were also elevated in cortices of Al-treated rats. These data are in contrast to the changes found in liver fractions where exposure to Fe greatly enhanced hepatic pro-oxidant events as judged by changes in all three of the test indices used. Concurrent treatment with Al did not potentiate the pro-oxidant effects of Fe in liver. Al treatment had very minor effects on hepatic parameters of oxidative events. The results suggest that the presence of Al may exert deleterious pro-oxidant changes within the brain, which may be related to induction of oxidant species. These changes are tissue-specific and appear to be independent of any promotion of pro-oxidant status induced by exogenous Fe.

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[d-Pen2,d-Pen5]Enkephalin, a δ opioid agonist, reduces endogenous aluminum content in the rat central nervous system

Cited by 5 publications

References 41 publications

Does neurotransmission impairment accompany aluminium neurotoxicity?

Does neurotransmission impairment accompany aluminium neurotoxicity?

The Role of δ-Opioid Receptors in Brain Ionic Homeostasis Under Physiological Condition

Aluminum but not iron treatment induces pro-oxidant events in the rat brain

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