الفهرس 
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Abstract
Acrylamide is a molecular monomer organic compound widely used all over the world in various applications as wastewater management, soil condition¬ers, dye synthesis, in laboratories for gel electrophoresis and the cosmetic paper, textile indus¬tries. However, it causes severe neurological damage in humans and experimental animals. This study was done to show the effects of melatonin and allicin on ACR-induced neuropathy in adult male albino rats.
The study was carried out on thirty-six rats which were randomly divided into six groups each consisting of ten rats as the following design:
group (Ia): Control rats fed on basal diet, distilled water ad libitum daily for 21 days.
group (Ib): Allicin treated group, the rats were treated orally with Allicin at dose (20mg/kg b. wt.)Daily for 21 days.
group (Ic): Melatonin treated group; the rats were treated orally day by day with melatonin (10mg/kg b. wt.) for 21days.
group (II): Acrylamide treated group; the rats were treated orally with Acrylamide at dose of (50 mg/kg b. wt.) dissolved in 5ml distilled water daily for 15 days for induction neuropathy.
group (III): Acrylamide and Allicin group, the rats were treated orally with Acrylamide at dose of (50 mg/kg b. wt.) and Allicin at dose (20mg/kg b. wt) a week before ACR administration.
group (VI): Acrylamide and Melatonin group, the rats were treated orally with Acrylamide at dose of (50 mg/kg b. wt.)Daily and melatonin (10mg/kg b. wt.) a week before ACR administration.
At the end of the experiment, blood samples were collected from retro-orbital vein and used for estimation of serum activity of TNF. Part of brain homogenate was used for estimation oxidant/ antioxidant status by estimation levels of MDA, 8-OHdG, total GSH, reduced GSH, GSSG and GSH/GSSG ratio .Also, for estimation AChE and brain neurotransmitters (Ach, Serotonin and dopamine).Finally , for estimation Brain nuclear factor erythroid-2 related factor-2 and amyloid protein (Nrf2 and AB1-42) and Gene expression of Nrf2 ,NFkB and Keap-1.
In this study, our results revealed that:
1. There is significant increase in the level of MDA and 8-OHdG in ACR-treated rats compared to control one which is indication for lipid and DNA oxidative damage of brain tissue. While, Rats treated with allicin or melatonin showed a non- significant increase in MDA with non- significant decrease in 8-OHdG compared to control one.
2. The administration of ACR at dose (50 mg/kg) b.wt resulted in a significant decrease in total GSH ,reduced GSH and GSH/GSSG ratio with significant increase in GSSG comparing to control. While co-admiration of ACR with melatonin ameliorated the level of total GSH, reduced GSH, GSSG and GSH/GSSG ratio when compared to the corresponding ones in ACR-group.
3. The co-admiration of ACR with allicin showed non- significant increase in total GSH level and GSH/GSSG ratio with significant increase in reduced GSH level and significant decrease in GSSG level when compared to the corresponding ones in ACR-group.
4. The activity of AChE was significantly increased in ACR -treated rats comparing with control which indicated the damage caused to Brain. on the other hand, treatment with allicin or melatonin significantly decreased this parameter compared with ACR-treated rats. While, Ach level was significantly decreased in ACR -treated rats comparing with control.
5. The co-administration of allicin or melatonin with ACR resulted in significant increase of Ach level when compared to the corresponding ones in ACR-group.
6. Serotonin and dopamine levels were significantly decreased in ACR-group compared with control one.
7. ACR-intoxicated rats treated with allicin showed a non-significant increase in brain serotonin level with significant increase in brain dopamine level comparable to ACR-challenged rats. While, treatment of ACR-intoxicated rats with melatonin significantly increased in brain serotonin and dopamine levels when compared to corresponding ones in ACR-challenged rats.
8. Administration of ACR at dose (50 mg/kg) b.wt resulted in significant increase in serum TNF-α level in ACR-treated group as compared to control. While, Co-treatment of ACR with allicin or melatonin resulted in a significant decrease in serum TNF-α level when compared to the respective values in ACR-treated rats.
9. The concentrations of amyloid protein in brain tissue was significantly increased in ACR-treated group comparing with control one. While, co-administration of allicin or melatonin with ACR group the concentration of AB1-42 was significantly decreased compared to ACR -treated group.
10. There is a significant decrease in brain Nrf2 level in ACR-treated group when compared to control ones.
11. The treatment of ACR-intoxicated rats with allicin non-significantly increased brain Nrf2 level. While, The treatment of ACR-intoxicated rats with melatonin significantly increased brain Nrf2 level when compared to ACR-treated group.
12. Gene expression of Nrf2 ,NF-kB and Keap-1 mRNA transcript in ACR- treated group were significantly increased in brain tissue as compared to control one.
13. The co-administration of allicin or melatonin with ACR significantly decreased Gene expression of Nrf2, NF-kB and Keap-1 mRNA transcript in brain tissue when compared with ACR-intoxicated rats.
14. The histopathological investigations in brain tissue revealed congested submeningeal blood vessels, hemorrhage and mild inflammatory cell infiltration in the meninges, neuropil spongiosis and neutrophagia in degenerated neutons in ACR-treated group. While, the microscopic examination of rats in (ACR+Allicin) -treated group showed congestion of both submeningeal and cortical blood vessels.While,other rats in(ACR+Melatonin)-treated group revealed congestion of cortical blood vessels.
15. The histopathological findings in some brain tissue of (ACR+Allicin) and (ACR+Melatonin)-treated groups revealed normal histological structure of the meninges and cerebrum cortex.