Curcumin counteracts the aluminum-induced ageing-related alterations in oxidative stress, Na+K+-ATPase and protein kinase C in adult and old rat brain regions. Biogerontology

School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.
Biogerontology (Impact Factor: 3.29). 12/2008; 10(4):489-502. DOI: 10.1007/s10522-008-9195-x
Source: PubMed


This study investigated the effect of curcumin on aluminium-induced alterations in ageing-related parameters: lipid peroxidation, superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-s-transferase (GST), protein kinase C (PKC), Na(+), K(+)-adenosine triphosphatase (Na(+), K(+)-ATPase) and acetylcholinesterase (AChE) in the cerebral cortex and hippocampus of the brain of 10- and 24-month-old rats. Measurements taken from aluminium-fed rats were compared with those from rats in which curcumin and aluminium were co-administered. In aluminium-treated rats the levels of lipid peroxidation, PKC and AChE were enhanced while the activities of SOD, GPx, GST and Na(+), K(+)-ATPase were significantly decreased in both the brain regions of both age-groups. In animals co-administered with curcumin and aluminium, the levels of lipid peroxidation, activities of PKC and AChE were significantly lowered while the activities of SOD, GPx, GST and Na(+), K(+)-ATPase were significantly enhanced in the two brain regions studied indicating curcumin's protective effects against aluminium toxicity. Though the magnitudes of curcumin-induced alterations varied in young and old animals, the results of the present study also demonstrated that curcumin exerts a protective effect against aluminium-induced elevation of ageing-related changes by modulating the extent of oxidative stress (by upregulating the activities of antioxidant enzymes) and by regulating the activities of Na(+), K(+) ATPase, PKC and AChE. Therefore, it is suggested that curcumin counters aluminium-induced enhancement in ageing-related processes.

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    • "Moreover, Al remains one of the most studied toxins affecting the nervous system. Some experts believe that Al crosses the blood–brain barrier, forming deposits in the brain and contributing to the formation of Alzheimer's-like neurofibrillary tangles (Sharma et al. 2009). Al exposure disrupts lipid membrane fluidity, perturbing iron, magnesium, and calcium homeostasis and causes oxidative stress (Mailloux et al. 2011). "
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    ABSTRACT: Aluminium (Al) is the most abundant metal in the earth's crust. Al exposure can cause a variety of adverse physiological effects in humans and animals. Our aim was to demonstrate that specific probiotic bacteria can play a special physiologically functional role in protection against Al toxicity in mice. Thirty strains of lactic acid bacteria (LAB) were tested for their aluminium-binding ability, aluminium tolerance, their antioxidative capacity, and their ability to survive the exposure to artificial gastrointestinal (GI) juices. Lactobacillus plantarum CCFM639 was selected for animal experiments because of its excellent performance in vitro. Forty mice were divided into four groups: control, Al only, Al plus CCFM639, and Al plus deferiprone (DFP). CCFM639 was administered at 10(9) CFU once daily for 10 days, followed by a single oral dose of aluminium chloride hexahydrate at 5.14 mg aluminium (LD50) for each mouse. The results showed that CCFM639 treatment led to a significant reduction in the mortality rates with corresponding decrease in intestinal aluminium absorption and in accumulation of aluminium in the tissues and amelioration of hepatic histopathological damage. This probiotic treatment also resulted in alleviation of hepatic, renal, and cerebral oxidative stress. The treatment of L. plantarum CCFM639 has potential as a therapeutic dietary strategy against acute aluminium toxicity.
    Full-text · Article · Nov 2015 · Applied Microbiology and Biotechnology
    • "Al is a commonly studied neurotoxin that affects the nervous system , including various regions of the brain (Nehru & Bhalla 2006). Some experts believe that Al crosses the blood–brain barrier and plays a role in the formation of Alzheimer-like neurofibrillary tangles (Sharma et al. 2009). Al +3 and other metals influence the oligomerization and conformational changes of the b-amyloid protein as a cross-linker in the 'amyloid cascade hypothesis', and therefore, their implications are important in this context. "
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    ABSTRACT: Aluminium (Al) toxicity is closely linked to the pathogenesis of Alzheimer's disease (AD). This experimental study investigated the neuroprotective effect of melatonin (Mel; 10 mg/kg bwt) on aluminium chloride (AlCl3 ; 34 mg/kg bwt) induced neurotoxicity and oxidative stress in rats. Adult male albino Wistar rats were injected with AlCl3 for 7 days. The effect on brain structure, lipid peroxidation (LPO), nitric oxide (NO) levels, glutathione (GSH) content, antioxidant enzymes (SOD, CAT, GPx and GR), apoptotic proteins (Bax and Bcl-2) and an apoptotic enzyme (caspase-3) was investigated. No apparent changes occurred following the injection of melatonin. Melatonin pretreatment of the AlCl3 -administered rats reduced brain damage, and the tissues appeared like those of the control rats. Compared to treatment with AlCl3 , pretreatment with melatonin decreased LPO and NO levels and increased the GSH content and antioxidant enzyme activity. Moreover, melatonin increased the levels of the anti-apoptotic protein, Bcl-2, decreased the levels of the pro-apoptotic protein, Bax, and inhibited caspase-3 activity. Therefore, our results indicate that melatonin may provide therapeutic value against aluminium-induced oxidative stress and histopathological alternations in the rat brain and that these effects may be related to anti-apoptotic and antioxidant activities. © 2015 The Authors. International Journal of Experimental Pathology © 2015 International Journal of Experimental Pathology.
    No preview · Article · Apr 2015 · International Journal of Experimental Pathology
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    • "Curcumin confers protection via antioxidant, anti-inflammatory (Huang et al., 1991), anti-microbial, anti-parasitic, anti-mutagen and anticancer properties (Conney et al., 1991). Antioxidant properties of curcumin are related to its powerful scavenging of superoxide anion, hydroxyl radical and nitric oxide (Sharma et al., 2008). The purpose of this study is to examine mechanism(s) of neurotoxicity as well as haematological changes induced by long term of Al treatment. "
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    ABSTRACT: Aluminium (Al) is a ubiquitous element introduced into the environment and is implicated in the pathogenesis of several neurological disorders associated with cognitive impairment. Free radical-mediated cytotoxicity is involved in Al detrimental effects, where the brain is a core target of Al toxicity being more vulnerable to oxidative damage as a result of its high lipid content. This work aims to evaluate the potential role of curcumin in modulating the neurobehavioral toxic action(s) induced experimentally by Al in rats, using ascorbic acid as reference treatment. Male adult Sprague Dawley rats were divided into seven groups; two control groups, administered distilled water and 9% ethanol. The other group were AlCl ³ (4.2mg/kg, i.p), ascorbic acid (85mg/kg, p.o) or curcumin (100 mg/kg, p.o) treated groups. In addition, ascorbic acid or curcumin was administered combined with Al in the last two groups. The different regimens were administered for 28 consecutive days. Rats were subjected to behavioral tests, namely open field and conditioned avoidance, then brain Al content as well as brain neurotransmitters contents [serotonin, norepinephrine and dopamine] were estimated. Markers of oxidative stress [brain reduced glutathione and malondialdehyde]; lactate dehydrogenase and acetylcholine esterase were also measured in the whole brain homogenate. In addition, haematological tests were performed by evaluating red blood cells count, haemoglobin concentration, and haematocrit %. In the open field, the latency time was increased in Al treated rats while the ambulation frequency, rearing and grooming were decreased. This inhibition in motor activity was accompanied by a decline in learning and memory performance in conditioned avoidance. Brain Al content increased while their content of 5-HT, NE and DA were suppressed. Lactate dehydrogenase activity and malondialdehyde content were elevated, while acetylcholine esterase activity and reduced glutathione concentration were reduced. Concomitant administration of curcumin restored all parameters measured, an effect that was comparable to ascorbic acid. In conclusion, curcumin may confer protection against Al induced neurobehavioral toxic effects through its decreased brain Al content, antioxidant action as well as restoration of neurotransmitter content, as evident by decreased LDH activity and obvious improvements of neurobehavioural tests.
    Full-text · Dataset · Oct 2013
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