Aluminium Phosphide Exposure: Implications on Rat Brain Lipid Peroxidation and Antioxidant Defence System

Dua, Raina; Gill, Kiran Dip

doi:10.1034/j.1600-0773.2001.d01-167.x

Cited by 88 publications

(65 citation statements)

References 20 publications

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“…In this study, basal levels of LPx products measured as malondialdehyde (MDA) were found to be significantly increased after Al exposure in both the cerebrum and cerebellum (Table 4). Similar results were also observed in various laboratories after Al treatment to experimental animals (Dua and Gill 2001;Kaiser et al 2005;Nehru et al 2007;Albendea et al 2007). It is known that Al is a nonredox active metal (Zatta et al 2002), therefore cannot participate directly in oxidation.…”

Section: Discussionsupporting

confidence: 89%

Protective Role of Lithium in Ameliorating the Aluminium-induced Oxidative Stress and Histological Changes in Rat Brain

Bhalla¹,

Dhawan²

2009

Cell Mol Neurobiol

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This study was carried out to investigate the effects of lithium (Li) supplementation on aluminium (Al) induced changes in antioxidant defence system and histoarchitecture of cerebrum and cerebellum in rats. Al was administered in the form of aluminium chloride (100 mg/kg b.wt./day, orally) and Li was given in the form of Li carbonate through diet (1.1 g/kg diet, daily) for a period of 2 months. Al treatment significantly enhanced the levels of lipid peroxidation and reactive oxygen species in both the cerebrum and cerebellum, which however were decreased following Li supplementation. The enzyme activities of catalase, superoxide dismutase (SOD) and glutathione reductase (GR) were significantly increased in both the regions following Al treatment. Li administration to Al-fed rats decreased the SOD, catalase and GR enzyme activities in both the regions; however, in cerebellum the enzyme activities were decreased in comparison to normal controls also. Further, the specific activity of glutathione-s-transferase and the levels of total and oxidized glutathione were significantly decreased in cerebrum and cerebellum following Al treatment, which however showed elevation upon Li supplementation. The levels of reduced glutathione were significantly decreased in cerebrum but increased in cerebellum following Al treatment, which however were normalized upon Li supplementation but in cerebellum only. Apart from the biochemical changes, disorganization in the layers of cerebrum and vacuolar spaces were also observed following Al treatment indicating the structural damage. Similarly, the loss of purkinje cells was also evident in cerebellum. Li supplementation resulted in an appreciable improvement in the histoarchitecture of both the regions. Therefore, the study shows that Li has a potential to exhibit neuroprotective role in conditions of Al-induced oxidative stress and be explored further to be treated as a promising drug against neurotoxicity.

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Section: Discussionsupporting

confidence: 89%

Protective Role of Lithium in Ameliorating the Aluminium-induced Oxidative Stress and Histological Changes in Rat Brain

Bhalla¹,

Dhawan²

2009

Cell Mol Neurobiol

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“…Lipid peroxidation gives evidence for the attack of cell membranes by the evolved free radicals (Ferrari, 2000). In addition, glutathione in its reduced form is the most abundant intracellular antioxidant and is involved in scavenging free radicals or serving as a substrate for glutathione peroxidase enzyme that catalyzes the detoxification of H 2 O 2 (Dua and Gill, 2001). In the present study, significant changes in GSH were observed in the three studied brain regions after the two routes of EUD-NPs administration.…”

Section: Discussionsupporting

confidence: 47%

Preliminary safety assessment of Eudragit® polymers nanoparticles administration in the rat brain

Abdel-Wahhab¹,

Joubert²,

Khadrawy

et al. 2017

J App Pharm Sci

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Although nanotechnology can provide useful carriers to protect successfully active agents, it is necessary to determine the possible toxicity of these technological products before any extensive use. The aim of the current study was to evaluate the effects on the nervous system of Eudragit ® polymers nanoparticles (EUD-Nps), considered as model of drug delivery carriers. Nile red-labeled EUD-NPs were prepared by a double emulsion/solvent evaporation technique. Male Sprague-Dawley rats were treated orally (PO) or intraperitoneally (IP) with a single dose of EUD-NPs (50 mg/kg bw). Animals were sacrificed after 4h, 48h, 1 week and 3 weeks and the brain of each rat was removed and dissected into the forebrain, midbrain and hindbrain regions. Acetylcholinesterase (AChE) activity, lipid peroxidation, reduced glutathione and nitric oxide were determined in different brain region homogenate. Other samples were used for the histological and fluorescent examinations. The results indicated that within the two routes of administration, all the tested parameters showed insignificant changes during the tested time intervals and all of them were in the normal range of the control by the 3 rd week. Moreover, the histological examination revealed a normal histological picture of the brain tissues after 3 weeks of administration. The fluorescent examination showed that EUD-NPs were found in the brain tissues at all the studied times. These findings showed that EUD-NPs have the ability to cross the blood brain barrier but induced little toxic effects on the brain. Further studies are needed to verify the fate of these NPs in the long term before using them as a vector.

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“…GSTs are essential components of the cellular antioxidant defence system, as they catalyze the conjugation of GSH to several dangerous compounds (Arrigo 1999;Rahaman et al 1999). As for the effect of metal ions on GST, conflicting results have so far been reported on both the activity and expression of the different GST classes in various tissues (Yousef 2004;Dua and Gill 2001).…”

Section: Introductionmentioning

confidence: 99%

Acute effects of cadmium on liver phase I and phase II enzymes and metallothionein accumulation on sea bream Sparus aurata

Bouraoui¹,

Bannı

Ghedira³

et al. 2007

Fish Physiol Biochem

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This research was designed to study Sparus aurata (sea bream) biotransformation and detoxification responses to acute exposure to cadmium (Cd). Sexually immature gilthead sea bream were treated by intraperitoneal injection of Cd chloride (200 microg kg(-1)) for 6, 12, 24 and 48 h. Cd accumulation was quantified in sea bream liver by graphite furnace atomic absorption spectroscopy after the various exposure periods. The following biological responses were measured: (1) ethoxyresorufin-O-deethylase (EROD) activity as phase I biotransformation parameter, (2) liver glutathione-S-transferase (GST) activity as a phase II conjugation enzyme and metallothionein (MT) content as specific response to Cd contamination. Cd bioaccumulation in the liver resulted in an increasing uptake up to 10.3 microg g(-1) wet weight after 48 h of exposure. EROD showed a significant activation only after 6 h exposure and a return to control levels after 12 h. GST revealed significant activation starting from 12 h exposure. MT accumulation in liver showed the same behavior as GST activation.

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Aluminium Phosphide Exposure: Implications on Rat Brain Lipid Peroxidation and Antioxidant Defence System

Cited by 88 publications

References 20 publications

Protective Role of Lithium in Ameliorating the Aluminium-induced Oxidative Stress and Histological Changes in Rat Brain

Protective Role of Lithium in Ameliorating the Aluminium-induced Oxidative Stress and Histological Changes in Rat Brain

Preliminary safety assessment of Eudragit® polymers nanoparticles administration in the rat brain

Acute effects of cadmium on liver phase I and phase II enzymes and metallothionein accumulation on sea bream Sparus aurata

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