Early Neuroprotective Effect of Nitric Oxide in Developing Rat Brain Irradiated in Utero

Gisone, Pablo; Boveris, Alberto; Dubner, Diana; Perez, Maria R; Robello, Elizabeth; Puntarulo, Susana

doi:10.1016/s0161-813x(02)00166-3

Cited by 18 publications

(13 citation statements)

References 55 publications

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“…6). The extra peak detected in DG which is not visible in the computer-simulated signal seems to be due to the formation of the complex Cu-MGD, as previously reported (Gisone et al, 2003) (Fig. 6, line d).…”

Section: Resultssupporting

confidence: 82%

Exposure to excess dissolved iron in vivo affects oxidative status in the bivalve Mya arenaria

González

Abele

Puntarulo

2010

Comparative Biochemistry and Physiology Part C: Toxicology &

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The effect of in vivo Fe exposure on the oxidative metabolism of the bivalve Mya arenaria was studied. Fe was supplemented in natural seawater and resulted in a significant increase in the total Fe content in the bivalve digestive gland (DG) between 9 to 17 days of exposure. Mortality of treated animals increased drastically after day 18. Oxidative stress conditions were characterized in DG through assessment of the generation of reactive oxygen species (ROS) and ascorbyl radical (A•) content. Both parameters were affected following a biphasic profile showing significant increases by days 2 and 9 of Fe exposure. The content of 2-thiobarbituric acid reactive substances (TBARS) was significantly increased over control values by days 2, 9 and 17 of treatment. The labile Fe pool (LIP) in isolated DG was elevated over control values by day 7, and maintained this increase until day 17 of Fe exposure. The content of NO, assessed by EPR spin trapping, was 60% lower in DG of animals exposed for 2 days to Fe than in control values, with no further changes. The biphasic profile of oxidative stress response to Fe exposure in DG suggests that at early stages of Fe supplementation the cellular control mechanisms, such as CAT activity, were operative to limit oxidative damage, but further Fe exposure overwhelmed these abilities. Moreover, the second phase could be understood as the consequence of the exhaustion of cellular protective systems that could also involve NO.

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Section: Resultssupporting

confidence: 82%

Exposure to excess dissolved iron in vivo affects oxidative status in the bivalve Mya arenaria

González

Abele

Puntarulo

2010

Comparative Biochemistry and Physiology Part C: Toxicology &

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“…Recent data indicate that in addition to the rapid burst of radicals and reactive oxigen species observed immediately following irradiation, cells can exhibit persistent and prolonged increases in reactive oxygen species/reactive nitrogen species detectable from several minutes to several days postirradiation. Growing evidence supports a role for reactive nitrogen species, particularly for NO in radiation-induced signaling mechanisms [51][52][53]. Therefore, it is possible that in our system the induction of NO by ␥-irradiation decreases HLA-G1 surface levels by proteolytic shedding through a metalloprotease-dependent mechanism.…”

Section: Discussionmentioning

confidence: 83%

Ionizing radiation modulates the surface expression of human leukocyte antigen-G in a human melanoma cell line

Michelin¹,

Gallegos²,

Dubner³

et al. 2009

Human Immunology

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“…An increase in the expression of the NO synthase gene (iNOS) stimulated by Cd has been demonstrated in vivo and in vitro[71] [72]. In addi-Journal of Behavioral and Brain Science tion, NO reacts with the superoxide ion ( 2 O − ) to form the ion peroxynitrite (ONOO − ), a very reactive toxic molecule involved in neurodegenerative pathologies, it acts as a powerful oxidant capable of modifying the functioning of proteins, nucleic acids (DNA oxidation) and lipids (LPO)[73] [74], which might explain the increase in LPO observed in our study. Once the LPO is provoked, it…”

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confidence: 99%

Effect of Chronic Administration of Cadmium on Anxiety-Like, Depression-Like and Memory Deficits in Male and Female Rats: Possible Involvement of Oxidative Stress Mechanism

Lamtai¹,

Chaibat²,

Ouakki³

et al. 2018

JBBS

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The main objective of this work is to study the effect of chronic administration of cadmium (Cd) on the level of depression-like, anxiety-like, memory state and oxidative stress in male and female Wistar rats. For this purpose, this study was conducted with 24 rats for each gender. Four groups were constituted: (Group 1: Control): received saline solution NaCl (0.9%), (Group 2: Cd-0.25; Group 3: Cd-0.5; Group 4: Cd-1): received daily 0.25 mg/kg, 0.5 mg/kg and 1 mg/kg of Cd respectively during 8 weeks. After treatment period, animals were tested in the open-field, elevated plus maze tests for anxiety-like behavior, and forced swimming test for depression-like behavior. The Y maze was used to evaluate the working memory and the Morris Water Maze, to evaluate space learning and spatial memory. The results revealed that in males, all doses of Cd provoke depression-like, while in females only the group treated with 1 mg/kg Cd shows elevated depression-like behavior. In regard to anxiety-like behavior, Cd induces an anxiogenic effect in both genders tests. In the Y-Maze test, both males and females expressed a low percentage of alternations, suggesting that working memory was affected by Cd at 1 mg/kg. In the Morris Water Maze test, the space learning and spatial memory were significantly impaired in the group Cd-1. Neurochemical analysis showed that levels of nitric oxide and lipid peroxidation in the hippocampus How to cite this paper: Lamtaiwere significantly increased after Cd treatments. Overall analysis of our data revealed that Cd caused significant alterations in the examined parameters that were sex-dependent and dose-dependent. IntroductionCd is one of the most toxic elements that bio-accumulates in the environment [1], especially in industrial areas via atmospheric dispersion and ground contamination surrounding metal emitting industries [2]. Cd may find its way to the human population through food and beverage, drinking water, air, and cigarette smoking. Although its toxicity is well established, the interaction of this element within a biological system and its resulting potential for harm is less well established. Cd has a long biological half-life mainly due to its low rate of excretion from the body [3].At peripheral level, prolonged exposure to Cd will cause toxic effect due to its accumulation over time in a variety of tissues, including kidneys, liver, central nervous system (CNS), and peripheral neuronal systems [4]. At central level, the transport of Cd through the blood-brain barrier (BBB) is the first step in regulating the entries of the metal into the CNS. Also, Cd can be taken from the nasal mucosa or olfactory pathways into the CNS [5]. It is well known in the CNS that the heavy metals, including Cd, act as catalysts for biochemical reactions, regulators of gene expression, second messengers in signaling pathways and cofactors for many vital enzymes, such pathways implicated in regulating physiological, pathological and behavioral functions. Chronical exposure to Cd affects many nervous syste...

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Early Neuroprotective Effect of Nitric Oxide in Developing Rat Brain Irradiated in Utero

Cited by 18 publications

References 55 publications

Exposure to excess dissolved iron in vivo affects oxidative status in the bivalve Mya arenaria

Exposure to excess dissolved iron in vivo affects oxidative status in the bivalve Mya arenaria

Ionizing radiation modulates the surface expression of human leukocyte antigen-G in a human melanoma cell line

Effect of Chronic Administration of Cadmium on Anxiety-Like, Depression-Like and Memory Deficits in Male and Female Rats: Possible Involvement of Oxidative Stress Mechanism

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