Aluminum induced encephalopathy in the rat

Lipman, Jonathan J.; Colowick, Sidney P.; Lawrence, Patricia L.; Abumrad, Naji N.

doi:10.1016/0024-3205(88)90385-2

Cited by 28 publications

(4 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Microscopic examination of the cerebral cortex In the group B (induced 0.2 MLS Alcl 3 ) only slight and mild distortions were observed in the architecture of the brain, the architecture of the brain in group C and D animals that were treated on higher dose (0.4 ml and 0.6mls respectively), a more prominent and significant damage was observed in the brain, it was also observed that animals in various groups demonstrated a dose-dependent damage in the cerebral cortex of aluminiumtreated rats as observed in this study. The histological alterations and distortions in the histo-architecture of the cortical layers in the treated rats and these findings are consistent with and corroborate the reports of previous studies [42,43,44] The alteration in the histological layers may have been the reason behind the reduction in weight of the brain across the aluminium treated group, which correlate with [45]. The finding from this study supports the hypothesis that aluminium has potential role in neurodegenerations [46].…”

Section: Discussionsupporting

confidence: 92%

Cerebral Cortical Damage in Adult Wistar Rats Following Aluminium Chloride Administration

Ajibade

Fakunle

Omoola

2019

AJRIMPS

View full text Add to dashboard Cite

This study investigated some effects of aluminium chloride on the cerebral cortex of adult Wistar rats. Aluminium chloride as one of the toxic metals has been known to be one of the major environmental pollutants across the world which has been reported in relation to Neurodegenerative diseases (ND) associated with metallic intoxication. It is present in many pharmaceutical drugs, food products and also used in the treatment of domestic water being involved in skeletal, haematological and neurological diseases. Thirty-two adult Wistar of both sexes weighing between 143 g-189 g were randomly grouped into four groups, group A, B, C and D each group containing 8 rats. Group A rats which were the controls, were maintained on standard feed (grower mash) and water for 21 days. Rats in group B, C and D were treated with 0.2 g/kg, 0.4 g/kg and 0.6 g/kg of aluminium chloride respectively for 21days. The aluminium chloride solution was administered orally on a daily basis for that period. The weight of the Wistar rats was recorded on a weekly basis (before and at the end of each week of administration). On the 22nd day the Wistar rats in group A, B, C and D were sacrificed by cervical dislocation, blood was collected through cardiac puncture, the brain was removed and weighed immediately using sensitive balance, part of the brain of all Wistar rats in each group was collected and homogenized for biochemical analysis, the remaining part was then fixed in 10% formol saline, the tissue was processed and sectioned at 5µm and stained with hematoxylin and eosin for histological study. Results showed that the mean body weights of the Wistar rats significantly increased in the treated groups when compared with the control group. The mean brain weights of the aluminium- treated groups showed insignificant decreased (P>0.05) when compared to the control group. In the biochemical analysis, there was a statistically significant increase (P<0.05) in the level of Malondialdehyde (MDA) in the aluminium-treated groups, and a significant decrease (P<0.05) in the level of Superoxide dismutase (SOD), and Succinate Dehydrogenase (SDH) in the aluminium treated group. Histological study of the brain (cerebral cortex) revealed that the cerebral cortical layers of the aluminium treated groups appeared distorted and degenerated, in a dose-dependent manner. The study concluded that aluminium chloride has a neurotoxic effect on the cerebral cortex of adult Wistar rats which invariably may alter some cerebral functions.

show abstract

Section: Discussionsupporting

confidence: 92%

Cerebral Cortical Damage in Adult Wistar Rats Following Aluminium Chloride Administration

Ajibade

Fakunle

Omoola

2019

AJRIMPS

View full text Add to dashboard Cite

show abstract

“…Indeed, indirect evidences exist that aluminum could alter glucose metabolism: 15 it inhibits utilization of glucose in the brain, hexokinase and G6PD, [43][44][45] and it reduces glucose uptake by cortical synaptosomes. 46 In the present paper, we have conrmed a high affinity of aluminum to G6P, with a very large number of possible compounds that could be formed depending on concentration conditions. We have seen the high affinity of forming mononuclear 1 : 1 species, some of them competitive with the formation of aluminum-citrate, one of the main low molecular mass chelators of aluminum in blood serum.…”

Section: Discussionmentioning

confidence: 89%

A computational study on interaction of aluminum withd-glucose 6-phosphate for various stoichiometries

Formoso

López

2017

RSC Adv.

View full text Add to dashboard Cite

show abstract

“…Of these, Al has been considered to be one of the most important factors (Kawahara 1999) contributing to the development of dialysis dementia (Alfrey et al 1976), Parkinson's disease (Good & Olanow 1992), amyotrophic lateral sclerosis (Yasui et al 1991), and AD (Hollosi et al 1994). Based on cumulative observations indicating that a neurotoxin was expressed when Al was parenterally administered to mammals (Clayton et al 1992;Lipman et al 1988), and those wherein hemodialysis patients exposed to high concentrations of Al showed a decline in their memory, attention, and concentration (Bolla et al 1992), Al accumulation in the brain was assumed to induce neuropathy, thereby developing the initial symptom of AD. Based on these results, we examined whether Al accumulation in the brain induces a memory deficit in animals by using a water maze task.…”

Section: Discussionmentioning

confidence: 98%

Memory Deficit in Mice Administered Aluminum–maltolate Complex

2006

View full text Add to dashboard Cite

Recently, aluminum (Al) has been identified as one of the environmental factors responsible for cause certain nerve degeneration diseases, particularly, Alzheimer's disease (AD). However, the relationship between Al and AD is controversial. We previously examined whether Al induced neurotoxin in the brain of mice when aluminum-maltolate complex (ALM) was administered daily for 120 days. Our results revealed that Al accumulated in the brain induced oxidative stress, and the nerve degeneration was detected in the brain of the ALM-treated group. On the basis of these results, we have tried to examine whether the incorporated Al affects memory in mice with regard to an indicator of spatial memory deficits depending on the chemical forms of Al, namely, as an ion (AlCl3) and in the form of a complex (ALM). We administered saline, AlCl3, and ALM at a concentration of 40 micromol Al/kg body weight to mice by daily ip injections for 60 days. We assessed spatial memory by a water maze task and determined the Al levels in the brain of the mice by the neutron activation analysis method. Spatial memory deficit as an indicator of the swimming time was related to Al accumulation in the brain of mice; the chemical form of the Al compound was important in order to exhibit the memory deficit in mice; the uptake of Al is higher in mice when it is administered in a complex form than in an ionic form.

show abstract

Aluminum induced encephalopathy in the rat

Cited by 28 publications

References 30 publications

Cerebral Cortical Damage in Adult Wistar Rats Following Aluminium Chloride Administration

Cerebral Cortical Damage in Adult Wistar Rats Following Aluminium Chloride Administration

A computational study on interaction of aluminum withd-glucose 6-phosphate for various stoichiometries

Memory Deficit in Mice Administered Aluminum–maltolate Complex

Contact Info

Product

Resources

About