Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hippocampal CA1 neurons exposed to a nonlethal period (2 min) of ischemia, acquired tolerance to a subsequent lethal 5-min period of ischemia, which usually causes delayed-type neuronal death. Intracellular Ca2+ movements before and after the 5 min of forebrain ischemia were evaluated in gerbil hippocampal CA1 pyramidal neurons, had acquired tolerance in comparison with nonischemia-tolerant CA1 neurons. Evaluation was performed by observing the ultrastructural intracellular Ca2+ distribution and the Ca2+ adenosine triphosphatase (Ca(2+)-ATPase) activity using electron microscopic cytochemistry. In comparison with nonischemia-tolerant CA1 neurons, mitochondria of ischemia-tolerant CA1 neurons sequestered more Ca2+ from the cytosomal fraction 15 min after the 5-min period of ischemia, and Ca2+ deposits in these mitochondria were rapidly decreased. Plasma membrane Ca(2+)-ATPase activities were already significantly elevated before the 5 min of ischemia, and remained at a higher level subsequently compared to nonischemia-tolerant CA1 neurons. Changes in the mitochondrial Ca2+ distribution and Ca(2+)-ATPase activities in ischemia-tolerant CA1 neurons after the 5-min period of ischemia showed a strong resemblance to those in CA3 neurons, which originally possess resistance to such periods of ischemia. These findings suggest that enhanced or maintained activities of mitochondrial Ca2+ sequenstration and plasma membrane Ca(2+)-ATPase reduced Ca2+ toxicity following 5-min ischemia in terms of time, resulting in escape from delayed neuronal death.
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PMID:Calcium movement in ischemia-tolerant hippocampal CA1 neurons after transient forebrain ischemia in gerbils. 878 35

With their widespread application in industry, agriculture, medicine, and daily life, rare earth elements (REEs) are widely used in various fields and eventually accumulated in human body. Therefore, understanding the effects of REEs on health has become more and more important. In this work, the neurotoxicity of lanthanum (La) was evaluated. Wistar rats were exposed to lanthanum chloride through oral administration at 0, 0.1, 2, and 40 mg/kg doses from gestation day 0 through 6 months of age. Experiments were carried out to reveal the effects of La exposure on brain functions from four aspects including behavioral performance, [Ca2+](i) level and the activity of Ca2+-ATPase (adenosine triphosphatase) in hippocampal cells, oxidative stress, and Nissl staining. Adverse effects were observed in 2 and 40 mg/kg dose groups and increased with dose. Morris water maze test showed that La exposure at 2 and 40 mg/kg could significantly impair the behavioral performance. (The preference for the target quadrant decreased by 16.6% and 19.4% versus control, respectively.) The neurotoxicological consequences demonstrated that the alteration in homeostasis of [Ca2+](i)/Ca2+-ATPase (the ratio of [Ca2+](i) vs. Ca2+-ATPase activity increased by 44% in rats of 40 mg/kg group), the inhibition to activities of antioxidant enzymes, and the subsequent cell damage (18% and 23% cell loss in CA3 subregion of rats in 2 and 40 mg/kg group, respectively) might be involved in the neurological adverse effects of REEs exposure.
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PMID:Neurotoxicological evaluation of long-term lanthanum chloride exposure in rats. 1831 42