Karema Abu-Elfotuh

Abstracts

4 Nephrotoxicity and Hepatotoxicity Induced by Chronic Aluminium Exposure in Rats: Impact of Nutrients Combination versus Social Isolation and Protein Malnutrition

Authors: Azza A. Ali, Karema Abu-Elfotuh, Doaa M. Abd El-Latif, Amany M. Gad, Yasser M. A. Elnahas

Abstract:

Background: Exposure to Aluminium (Al) has been increased recently. It is found in food products, food additives, drinking water, cosmetics and medicines. Chronic consumption of Al causes oxidative stress and has been implicated in several chronic disorders. Liver is considered as the major site for detoxification while kidney is involved in the elimination of toxic substances and is a target organ of metal toxicity. Social isolation (SI) or protein malnutrition (PM) also causes oxidative stress and has negative impact on Al-induced nephrotoxicity as well as hepatotoxicity. Coenzyme Q10 (CoQ10) is a powerful intracellular antioxidant with mitochondrial membrane stabilizing ability while wheat grass is a natural product with antioxidant, anti-inflammatory and different protective activities, cocoa is also potent antioxidants and can protect against many diseases. They provide different degrees of protection from the impact of oxidative stress. Objective: To study the impact of social isolation together with Protein malnutrition on nephro- and hepato-toxicity induced by chronic Al exposure in rats as well as to investigate the postulated protection using a combination of Co Q10, wheat grass and cocoa. Methods: Eight groups of rats were used; four served as protected groups and four as un-protected. Each of them received daily for five weeks AlCl3 (70 mg/kg, IP) for Al-toxicity model groups except one group served as control. Al-toxicity model groups were divided to Al-toxicity alone, SI- associated PM (10% casein diet) and Al- associated SI&PM groups. Protection was induced by oral co-administration of CoQ10 (200mg/kg), wheat grass (100mg/kg) and cocoa powder (24mg/kg) combination together with Al. Biochemical changes in total bilirubin, lipids, cholesterol, triglycerides, glucose, proteins, creatinine and urea as well as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate deshydrogenase (LDH) were measured in serum of all groups. Specimens of kidney and liver were used for assessment of oxidative parameters (MDA, SOD, TAC, NO), inflammatory mediators (TNF-α, IL-6β, nuclear factor kappa B (NF-κB), Caspase-3) and DNA fragmentation in addition to evaluation of histopathological changes. Results: SI together with PM severely enhanced nephro- and hepato-toxicity induced by chronic Al exposure. Co Q10, wheat grass and cocoa combination showed clear protection against hazards of Al exposure either alone or when associated with SI&PM. Their protection were indicated by the significant decrease in Al-induced elevations in total bilirubin, lipids, cholesterol, triglycerides, glucose, creatinine and urea levels as well as ALT, AST, ALP, LDH. Liver and kidney of the treated groups also showed significant decrease in MDA, NO, TNF-α, IL-6β, NF-κB, caspase-3 and DNA fragmentation, together with significant increase in total proteins, SOD and TAC. Biochemical results were confirmed by the histopathological examinations. Conclusion: SI together with PM represents a risk factor in enhancing nephro- and hepato-toxicity induced by Al in rats. CoQ10, wheat grass and cocoa combination provide clear protection against nephro- and hepatotoxicity as well as the consequent degenerations induced by chronic Al-exposure even when associated with the risk of SI together with PM.

Keywords: Aluminum, nephrotoxicity, hepatotoxicity, coenzyme Q10, cocoa, wheatgrass, isolation and protein malnutrition, nutrients combinations

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3 The Potential Role of Some Nutrients and Drugs in Providing Protection from Neurotoxicity Induced by Aluminium in Rats

Authors: Azza A. Ali, Abeer I. Abd El-Fattah, Karema Abu-Elfotuh, Shaimaa S. Hussein, Hanan A. Abd El-Samea

Abstract:

Background: Aluminium (Al) represents an environmental risk factor. Exposure to high levels of Al causes neurotoxic effects and different diseases. Vinpocetine is widely used to improve cognitive functions, it possesses memory-protective and memory-enhancing properties and has the ability to increase cerebral blood flow and glucose uptake. Cocoa bean represents a rich source of iron as well as a potent antioxidant. It can protect from the impact of free radicals, reduces stress as well as depression and promotes better memory and concentration. Wheatgrass is primarily used as a concentrated source of nutrients. It contains vitamins, minerals, carbohydrates, amino acids and possesses antioxidant and anti-inflammatory activities. Coenzyme Q10 (CoQ10) is an intracellular antioxidant and mitochondrial membrane stabilizer. It is effective in improving cognitive disorders and has been used as anti-aging. Zinc is a structural element of many proteins and signaling messenger that is released by neural activity at many central excitatory synapses. Objective: To study the role of some nutrients and drugs as Vinpocetine, Cocoa, Wheatgrass, CoQ10 and Zinc against neurotoxicity induced by Al in rats as well as to compare between their potency in providing protection. Methods: Seven groups of rats were used and received daily for three weeks AlCl3 (70 mg/kg, IP) for Al-toxicity model groups except for the control group which received saline. All groups of Al-toxicity model except one group (non-treated) were co-administered orally together with AlCl3 the following treatments; Vinpocetine (20mg/kg), Cocoa powder (24mg/kg), Wheat grass (100mg/kg), CoQ10 (200mg/kg) or Zinc (32mg/kg). Biochemical changes in the rat brain as acetyl cholinesterase (ACHE), Aβ, brain derived neurotrophic factor (BDNF), inflammatory mediators (TNF-α, IL-1β), oxidative parameters (MDA, SOD, TAC) were estimated for all groups besides histopathological examinations in different brain regions. Results: Neurotoxicity and neurodegenerations in the rat brain after three weeks of Al exposure were indicated by the significant increase in Aβ, ACHE, MDA, TNF-α, IL-1β, DNA fragmentation together with the significant decrease in SOD, TAC, BDNF and confirmed by the histopathological changes in the brain. On the other hand, co-administration of each of Vinpocetine, Cocoa, Wheatgrass, CoQ10 or Zinc together with AlCl3 provided protection against hazards of neurotoxicity and neurodegenerations induced by Al, their protection were indicated by the decrease in Aβ, ACHE, MDA, TNF-α, IL-1β, DNA fragmentation together with the increase in SOD, TAC, BDNF and confirmed by the histopathological examinations of different brain regions. Vinpocetine and Cocoa showed the most pronounced protection while Zinc provided the least protective effects than the other used nutrients and drugs. Conclusion: Different degrees of protection from neurotoxicity and neuronal degenerations induced by Al could be achieved through the co-administration of some nutrients and drugs during its exposure. Vinpocetine and Cocoa provided the most protection than Wheat grass, CoQ10 or Zinc which showed the least protective effects.

Keywords: rats, Aluminum, zinc, neurotoxicity, coenzyme Q10, cocoa, vinpocetine, wheat grass

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2 Comparative Study on the Influence of Different Drugs against Aluminium- Induced Nephrotoxicity and Hepatotoxicity in Rats

Authors: Azza A. Ali, Toqa M. Elnahhas, Abeer I. Abd El-Fattah, Mona M. Kamal, Karema Abu-Elfotuh

Abstract:

Background: Environmental pollution with the different aluminium (Al) containing compounds especially those in industrial waste water exposes people to higher than normal levels of Al that represents an environmental risk factor. Cosmetics, Al ware, and containers are also sources of Al besides some foods and food additives. In addition to its known neurotoxicity, Al affects other body structures like skeletal system, blood cells, liver and kidney. Accumulation of Al in kidney and liver induces nephrotoxicity and hepatotoxicity. Coenzyme Q10 (CoQ10) is a pseudo-vitamin substance primarily present in the mitochondria. It is a powerful antioxidant and acts as radical scavenger. Wheat grass is a natural product that contains carbohydrates, proteins, vitamins, minerals, enzymes and has antioxidant, anti-inflammatory, anticancer and cardiovascular protection activities. Cocoa is an excellent source of iron, potent antioxidants and can protect against many diseases. Vinpocetine is an antioxidant and anti inflammatory while zinc is an essential trace element involved in cell division and its deficiency is observed in many types of liver disease. Objective: To evaluate and compare the potency of different drugs (CoQ10, wheatgrass, cocoa, vinpocetine and zinc) against nephro- and hepato-toxicity induced by Al in rats. Methods: Rats were divided to seven groups and received daily for three weeks either saline for control group or AlCl3 (70 mg/kg, IP) for Al-toxicity model groups. Five groups of Al-toxicity model (treated groups) were orally received together with Al each of the following; CoQ10 (200mg/kg), wheat grass (100mg/kg), cocoa powder (24mg/kg), vinpocetine (20mg/kg) or zinc (32mg/kg). Biochemical changes in the serum level of Alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate deshydrogenase (LDH) as well as total bilirubin, lipids, cholesterol, triglycerides, glucose, proteins, creatinine and urea were measured. Liver and kidney specimens from all groups were also collected for the assessment of hepatic and nephrotic level of inflammatory mediators (TNF-α, IL-6β, nuclear factor kappa B (NF-κB), Caspase-3, oxidative parameters (MDA, SOD, TAC, NO) and DNA fragmentation. Histopathological changes in liver and kidney were also evaluated. Results: Three weeks of AlCl3 (70 mg/kg, IP) exposure induced nephro- and hepato-toxicity in rats. Treatment by the all used drugs showed protection against hazards of AlCl3. The protective effects were indicated by the significant decrease in ALT, AST, ALP, LDH as well as total bilirubin, lipids, cholesterol, triglycerides, glucose, creatinine and urea levels which were increased by Al. Liver and kidney of the treated groups showed decrease in MDA, NO, TNF-α, IL-6β, NF-κB, caspase-3 and DNA fragmentation which were increased by Al, together with significant increase in total proteins, SOD and TAC which were decreased by Al. The protection against both nephro- and hepato-toxicity was more pronounced especially with CoQ10 and wheat grass than the other used drugs. Histopathological examinations confirmed the biochemical results of toxicity and of protection. Conclusion: Protection from nephrotoxicity, hepatotoxicity and the consequent degenerations induced by Al can be achieved by using different drugs as CoQ10, wheatgrass, cocoa, vinpocetine and zinc, but CoQ10 as well as wheat grass possesses the most superior protection.

Keywords: Aluminum, nephrotoxicity, hepatotoxicity, zinc, coenzyme Q10, cocoa, wheatgrass, vinpocetine

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1 Influence of Protein Malnutrition and Different Stressful Conditions on Aluminum-Induced Neurotoxicity in Rats: Focus on the Possible Protection Using Epigallocatechin-3-Gallate

Authors: Azza A. Ali, Mona M. Kamal, Karema Abu-Elfotuh, Asmaa Abdelaty, Mona G. Khalil

Abstract:

Background: Aluminium (Al) is known as a neurotoxin environmental pollutant that can cause certain diseases as Dementia, Alzheimer's disease, and Parkinsonism. It is widely used in antacid drugs as well as in food additives and toothpaste. Stresses have been linked to cognitive impairment; Social isolation (SI) may exacerbate memory deficits while protein malnutrition (PM) increases oxidative damage in cortex, hippocampus and cerebellum. The risk of cognitive decline may be lower by maintaining social connections. Epigallocatechin-3-gallate (EGCG) is the most abundant catechin in green tea and has antioxidant, anti-inflammatory and anti-atherogenic effects as well as health-promoting effects in CNS. Objective: To study the influence of different stressful conditions as social isolation, electric shock (EC) and inadequate Nutritional condition as PM on neurotoxicity induced by Al in rats as well as to investigate the possible protective effect of EGCG in these stressful and PM conditions. Methods: Rats were divided into two major groups; protected group which was daily treated during three weeks of the experiment by EGCG (10 mg/kg, IP) or non-treated. Protected and non-protected groups included five subgroups as following: One normal control received saline and four Al toxicity groups injected daily for three weeks by ALCl3 (70 mg/kg, IP). One of them served as Al toxicity model, two groups subjected to different stresses either by isolation as mild stressful condition (SI-associated Al toxicity model) or by electric shock as high stressful condition (EC- associated Al toxicity model). The last was maintained on 10% casein diet (PM -associated Al toxicity model). Isolated rats were housed individually in cages covered with black plastic. Biochemical changes in the brain as acetyl cholinesterase (ACHE), Aβ, brain derived neurotrophic factor (BDNF), inflammatory mediators (TNF-α, IL-1β), oxidative parameters (MDA, SOD, TAC) were estimated for all groups. Histopathological changes in different brain regions were also evaluated. Results: Rats exposed to Al for three weeks showed brain neurotoxicity and neuronal degenerations. Both mild (SI) and high (EC) stressful conditions as well as inadequate nutrition (PM) enhanced Al-induced neurotoxicity and brain neuronal degenerations; the enhancement induced by stresses especially in its higher conditions (ES) was more pronounced than that of inadequate nutritional conditions (PM) as indicated by the significant increase in Aβ, ACHE, MDA, TNF-α, IL-1β together with the significant decrease in SOD, TAC, BDNF. On the other hand, EGCG showed more pronounced protection against hazards of Al in both stressful conditions (SI and EC) rather than in PM .The protective effects of EGCG were indicated by the significant decrease in Aβ, ACHE, MDA, TNF-α, IL-1β together with the increase in SOD, TAC, BDNF and confirmed by brain histopathological examinations. Conclusion: Neurotoxicity and brain neuronal degenerations induced by Al were more severe with stresses than with PM. EGCG can protect against Al-induced brain neuronal degenerations in all conditions. Consequently, administration of EGCG together with socialization as well as adequate protein nutrition is advised especially on excessive Al-exposure to avoid the severity of its neuronal toxicity.

Keywords: Environmental Pollution, rats, Aluminum, social isolation, neuronal degeneration, protein malnutrition, epigallocatechin-3-gallate

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