10497

PREVENTION OF ALUMINIUM TOXICITY AND OXIDATIVE DAMAGE BY MELATONIN IN BRAIN OVARIECTOMIZED FEMALE RATS

Article

Last updated: 03 Jan 2025

Subjects

-

Tags

Botany
Microbiology
Zoology

Abstract

Aluminium (AL) is an important element with known toxicity in human body, mainly in the centeral nervous system. Melatonin is known as antioxidant, free radical scaverger and metal chelator. The aim of this study to determine the effect of oral administration of melatonin on accumulation and toxicity of Alclз in brain of ovariectomized female rats. Orally administerated of Alcl3 at dose (10mg/Kg b.w.) for 8 weeks showed significant decrease in total protein,acetylcholenesterase(AchE) and glutathione content in brain tissues. While the lipid peroxidation Lpo, triglycerides Trig, total cholesterol  and phospholipids showed significant Increase. The treatment with melatonin at dose (5mg/kgb.w.) for 8 weeks showed slightly decreased pervious parameters.These data indicated that  orally treatment with melatonin against Alcl3 is probably responsible for preventaion of oxidative damage and Al-toxicity induced injury to brain of  experimental rats.

DOI

10.21608/absb.2008.10497

Keywords

Aluminium toxicity, oxidative damage, Brain

Authors

First Name

AMIRA

Last Name

MERSAL

MiddleName

-

Affiliation

Department of zoology, Faculty of Science,(girls) Al-Azhar University.

Email

-

City

-

Orcid

-

Volume

19

Article Issue

Issue 1-C

Related Issue

2050

Issue Date

2008-06-01

Receive Date

2008-01-01

Publish Date

2008-06-01

Page Start

15

Page End

26

Print ISSN

1110-2535

Online ISSN

2636-3305

Link

https://absb.journals.ekb.eg/article_10497.html

Detail API

https://absb.journals.ekb.eg/service?article_code=10497

Order

2

Type

Original Article

Type Code

520

Publication Type

Journal

Publication Title

Al-Azhar Bulletin of Science

Publication Link

https://absb.journals.ekb.eg/

MainTitle

PREVENTION OF ALUMINIUM TOXICITY AND OXIDATIVE DAMAGE BY MELATONIN IN BRAIN OVARIECTOMIZED FEMALE RATS

Details

Type

Article

Created At

22 Jan 2023