The inhibitory effect of aluminium on the (Na+/K+)ATPase activity of rat brain cortex synaptosomes

Silva, Virgília S.; Gonçalves, Paula P.

doi:10.1016/s0162-0134(03)00257-5

Cited by 27 publications

(23 citation statements)

References 73 publications

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“…Negative impacts on gill NKA activity are consistent with previous studies examining effects of long-term (weeks-months) acid/Al exposure on Atlantic salmon smolts (Staurnes et al, 1993;Magee et al, 2003). Decreased gill NKA activity may be attributed to increased chloride cell death via apoptosis and necrosis (Verbost et al, 1995), to the direct inhibition of enzyme activity by Al ions (Silva and Goncalves, 2003), or to the increased appearance of immature gill chloride cells with low levels of NKA protein (Wendelaar Bonga et al, 1990). Interestingly, gill NKA activity of smolts held at RR was significantly greater than T = 0 smolts after 6 days which may reflect the seasonal rise in gill NKA activity that occurs in smolts during the spring.…”

Section: Discussionsupporting

confidence: 84%

Impacts of short-term acid and aluminum exposure on Atlantic salmon (Salmo salar) physiology: A direct comparison of parr and smolts

Monette

McCormick

2008

Aquatic Toxicology

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Episodic acidification resulting in increased acidity and inorganic aluminum (Al i ) is known to impact anadromous salmonids and has been identified as a possible cause of Atlantic salmon population decline. Sensitive life-stages such as smolts may be particularly vulnerable to impacts of short-term (days-week) acid/Al exposure, however the extent and mechanism(s) of this remain unknown. To determine if Atlantic salmon smolts are more sensitive than parr to short-term acid/Al, parr and smolts held in the same experimental tanks were exposed to control (pH 6.3-6.6, 11-37 g l −1 Al i ) and acid/Al (pH 5.0-5.4, 43-68 g l −1 Al i ) conditions in the lab, and impacts on ion regulation, stress response and gill Al accumulation were examined after 2 and 6 days. Parr and smolts were also held in cages for 2 and 6 days in a reference (Rock River, RR) and an acid/Al-impacted tributary (Ball Mountain Brook, BMB) of the West River in Southern Vermont. In the lab, losses in plasma Cl − levels occurred in both control parr and smolts as compared to fish sampled prior to the start of the study, however smolts exposed to acid/Al experienced additional losses in plasma Cl − levels (9-14 mM) after 2 and 6 days, and increases in plasma cortisol (4.3-fold) and glucose (2.9-fold) levels after 6 days, whereas these parameters were not significantly affected by acid/Al in parr. Gill Na + ,K + -ATPase (NKA) activity was not affected by acid/Al in either life-stage. Both parr and smolts held at BMB (but not RR) exhibited declines in plasma Cl − , and increases in plasma cortisol and glucose levels; these differences were significantly greater in smolts after 2 days but similar in parr and smolts after 6 days. Gill NKA activity was reduced 45-54% in both life-stages held at BMB for 6 days compared to reference fish at RR. In both studies, exposure to acid/Al resulted in gill Al accumulation in parr and smolts, with parr exhibiting two-fold greater gill Al than smolts after 6 days. Our results indicate that smolts are more sensitive than parr to short-term acid/Al. Increased sensitivity of smolts appears to be independent of a reduction in gill NKA activity and greater gill Al accumulation. Instead, increased sensitivity of smolts is likely a result of both the acquisition of seawater tolerance while still in freshwater and heightened stress responsiveness in preparation for seawater entry and residence.

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Section: Discussionsupporting

confidence: 84%

Impacts of short-term acid and aluminum exposure on Atlantic salmon (Salmo salar) physiology: A direct comparison of parr and smolts

Monette

McCormick

2008

Aquatic Toxicology

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“…Besides, evidences reported suggest that Al may act in the neurotoxic action of amyloid beta-peptide (Ab) [46,47], the principal component of senile plaques, which are characteristics of AD [48].…”

Section: Discussionmentioning

confidence: 99%

Effect of Long-Term Exposure to Aluminum on the Acetylcholinesterase Activity in the Central Nervous System and Erythrocytes

et al. 2008

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Aluminum (Al), a neurotoxic agent, has been associated with Alzheimer's disease (AD), which is characterized by cholinergic dysfunction in the central nervous system. In this study, we evaluated the effect of long-term exposure to aluminum on acetylcholinesterase (AChE) activity in the central nervous system in different brain regions, in synaptosomes of the cerebral cortex and in erythrocytes. The animals were loaded by gavage with AlCl(3) 50 mg/kg/day, 5 days per week, totalizing 60 administrations. Rats were divided into four groups: (1) control (C); (2) 50 mg/kg of citrate solution (Ci); (3) 50 mg/kg of Al plus citrate (Al + Ci), and (4) 50 mg/kg of Al (Al). AChE activity in striatum was increased by 15% for Ci, 19% for Al + Ci and 30% for Al, when compared to control (P < 0.05). The activity in hypothalamus increased 23% for Ci, 26% for Al + Ci and 28% for Al, when compared to control (P < 0.05). AChE activity in cerebellum, hippocampus and cerebral cortex was decreased by 11%, 23% and 21% respectively, for Al, when compared to the respective controls (P < 0.05). AChE activity in synaptosomes was increased by 14% for Al, when compared to control (P < 0.05). Erythrocyte AChE activity was increased by 17% for Al + Ci and 11% for Al, when compared to control (P < 0.05). These results indicate that Al affects at the same way AChE activity in the central nervous system and erythrocyte. AChE activity in erythrocytes may be considered a marker of easy access of the central cholinergic status.

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“…The high-affinity choline transport by cholinergic presynaptic nerve terminals is hemicholinium-3-sensitive (K i ≈ 10 −9 to 10 −7 M) and driven by the transmembrane Na + gradient (Kuhar and Zarbin, 1978;Vickroy et al, 1985;Chatterjee et al, 1987;Saltarelli et al, 1987;Happe and Murrin, 1993;Okuda et al, 2000;Misawa et al, 2001), which is maintained by the (Na + /K + )ATPase (Stein, 1990;Nelson and Lill, 1994). During the last 20 years, a number of reports appeared to emphasize that in vivo and in vitro exposure of mammalian preparations to aluminum inhibits this P-type ATPase, a ubiquitous integral membrane pump of the plasma membrane (Lai et al, 1980;King et al, 1983;Rao, 1990Rao, , 1992Caspers et al, 1993Caspers et al, , 1994Lal et al, 1993;Sarin et al, 1997;Silva and Gonçalves, 2003;Silva et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Comparative effects of aluminum and ouabain on synaptosomal choline uptake, acetylcholine release and (Na+/K+)ATPase

Silva¹,

Nunes²,

Cordeiro³

et al. 2007

Toxicology

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The inhibitory effect of aluminium on the (Na+/K+)ATPase activity of rat brain cortex synaptosomes

Cited by 27 publications

References 73 publications

Impacts of short-term acid and aluminum exposure on Atlantic salmon (Salmo salar) physiology: A direct comparison of parr and smolts

Impacts of short-term acid and aluminum exposure on Atlantic salmon (Salmo salar) physiology: A direct comparison of parr and smolts

Effect of Long-Term Exposure to Aluminum on the Acetylcholinesterase Activity in the Central Nervous System and Erythrocytes

Comparative effects of aluminum and ouabain on synaptosomal choline uptake, acetylcholine release and (Na+/K+)ATPase

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