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1.
Pak J Pharm Sci ; 33(6(Supplementary)): 2785-2791, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-33879438

RESUMO

Exposure to cadmium has been extensively increased due to its usage in modern daily life. Inside the human body it induces deteriorating effects in every vital organ including brain. Oxidative stress has been widely implicated in neurotoxicity induced by cadmium exposure. Consumption of dietary source of exogenous antioxidants is one of the recommended ways to extenuate heavy metal-induced oxidative stress. The potential of nuts against heavy-metal induced neurotoxicity has not been investigated earlier. This study was, therefore, conducted to find out the antioxidant ability of almond and walnut in the prevention of cadmium-induced oxidative stress. Rats were treated with nuts (400 mg/kg) daily for 28 days whereas, cadmium (50 mg/kg) was given once in a week. Brain function was monitored in terms of memory performance using Morris water maze and elevated plus maze. Moreover, oxidative stress status was also evaluated. Results showed that weekly exposure of cadmium significantly reduced %memory retention, increased lipid per oxidation and inhibited antioxidant enzymes activity. When nuts supplemented rats were monitored for these parameters, it was observed that almond and walnut have a great potential to reduce cadmium-induced neurotoxicity as evident by decreased oxidative stress and improved memory function in cadmium intoxicated rats.


Assuntos
Antioxidantes/farmacologia , Encéfalo/efeitos dos fármacos , Cádmio/toxicidade , Juglans , Estresse Oxidativo/efeitos dos fármacos , Prunus dulcis , Animais , Catalase/metabolismo , Suplementos Nutricionais , Glutationa Peroxidase/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Memória/efeitos dos fármacos , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismo
2.
Acta Neurobiol Exp (Wars) ; 79(2): 169-183, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31342953

RESUMO

Cadmium, a heavy metal with no physiological function in the human body, is considered a bio-hazard. It is also considered to be a potent neurotoxin. The primary sources of cadmium exposure are diet and cigarette smoke. It has been postulated that nutritional deficiencies can increase the risk of cadmium toxicity. Nuts provide essential nutrients which are necessary for the maintenance of brain health in humans. The present study was designed to investigate the possible protective effects of almond and walnut supplementation on cadmium-induced neurotoxicity. Cadmium was orally administered at a dose of 50 mg/kg weekly with or without the supplementation of almond and walnut in rats. Intensities of depression­ and anxiety-related behaviors were assessed by the forced swim test and light/dark transition test, respectively. Memory function was also evaluated by the elevated plus maze, Morris water maze and novel object recognition task. After four weeks of treatment it was observed that cadmium administration significantly induced depressogenic and anxiogenic behaviors. Memory function was also impaired by cadmium administration. Cadmium-treated rats exhibited reduced noradrenalin, dopamine and serotonin levels in the brain, whereas the levels of their respective metabolites were significantly increased. The dietary supplementation of almond and walnut at a dose of 400 mg/kg/day significantly attenuated cadmium-induced depression, anxiety and memory impairments. Neurochemical aberrations also normalized following supplementation with these nuts in rats. The present study demonstrates that long-term supplementation with almond and walnut provides essential nutrients which may overcome nutritional deficiencies and thereby reduce heavy-metal intoxication.


Assuntos
Encéfalo/efeitos dos fármacos , Cádmio/toxicidade , Aprendizagem em Labirinto/efeitos dos fármacos , Memória/efeitos dos fármacos , Animais , Juglans , Memória/fisiologia , Transtornos da Memória/induzido quimicamente , Síndromes Neurotóxicas/tratamento farmacológico , Nozes , Ratos , Ratos Wistar
3.
Pak J Pharm Sci ; 31(5(Supplementary)): 2179-2184, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30393230

RESUMO

Major depressive disorder (MDD) is the leading cause of memory impairment in general population. The serotonin hypothesis provides a target model for the treatment of depression and depression-associated memory loss. 5-HT-1B receptor is suggested as a potential candidate in the pathophysiology of depressive illness. Dysfunction of 5-HT-1B receptors has been observed previously in depressive patients. Zolmitriptan, 5-HT-1B agonist is clinically recommended for the treatment of migraine. However, in present study this drug was tested as a potential treatment for depression and associated memory loss by altering the serotonergic function at receptor level. Rats (n=24) were equally divided into unstressed and stressed groups. Depression was induced by 19 days of restraint stress for 4 h which was followed by forced swim test and pattern separation test to assess depressive symptoms and memory impairment, respectively. The initial sign of depression-associated memory loss involves impaired pattern separation which is regarded as pseudodementia. In this study stressed rats showed depression- and pseudodementia-like symptoms. After the induction of depression, rats were treated with zolmitriptan at a dose of 0.3 mg/kg which resulted in a significant attenuation of depression and depression-associated memory impairment. Results are discussed with reference to the modulation of function of 5-HT-1B receptor following the administration of exogenous agonist.


Assuntos
Depressão/tratamento farmacológico , Depressão/psicologia , Transtornos Autoinduzidos/tratamento farmacológico , Transtornos Autoinduzidos/psicologia , Oxazolidinonas/uso terapêutico , Agonistas do Receptor 5-HT1 de Serotonina/uso terapêutico , Triptaminas/uso terapêutico , Animais , Depressão/complicações , Transtornos Autoinduzidos/etiologia , Masculino , Ratos , Ratos Wistar
4.
Pak J Pharm Sci ; 30(1 Suppl): 273-279, 2017 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-28625954

RESUMO

Excessive exposure of cadmium which is regarded as a neurotoxin can stimulate aging process by inducing abnormality in neuronal function. It has been reported that supplementation of almond and walnut attenuate age-related memory loss. Present study was designed to investigate the weekly administration of cadmium for one month on learning and memory function with relation to cholinergic activity. Cadmium was administered at the dose of 50 mg/kg/week. Whereas, almond and walnut was supplemented at the dose of 400 mg/kg/day along with cadmium administration to separate set of rats. At the end of experiment, memory function was assessed by Morris water maze, open field test and novel object recognition test. Results of the present study showed that cadmium administration significantly reduced memory retention. Reduced acetylcholine levels and elevated acetyl cholinesterase activity were also observed in frontal cortex and hippocampus of cadmium treated rats. Malondialdehyde levels were also significantly increased following the administration of cadmium. Daily supplementation of almond and walnut for 28 days significantly attenuated cadmium-induced memory impairment in rats. Results of the present study are discussed in term of cholinergic activity in cadmium-induced memory loss and its attenuation by nuts supplementation in rats.


Assuntos
Cádmio/administração & dosagem , Colinérgicos/administração & dosagem , Habituação Psicofisiológica/efeitos dos fármacos , Hipocampo/efeitos dos fármacos , Transtornos da Memória/induzido quimicamente , Transtornos da Memória/dietoterapia , Memória/efeitos dos fármacos , Acetilcolina/metabolismo , Envelhecimento/efeitos dos fármacos , Animais , Suplementos Nutricionais , Juglans , Aprendizagem em Labirinto/efeitos dos fármacos , Prunus dulcis , Ratos , Ratos Wistar
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