2012
DOI: 10.15208/mhsj.2012.68
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Preventive activity of ascorbic acid on lead acetate induced cerebellar damaged in adult Wistar rats

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Cited by 8 publications
(3 citation statements)
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“…Compared to the control group, prior treatment with vitamin C, when any tested metal was present, avoided the negative influences of heavy metals on the liver's function measures. Through creating inert complexes and reducing lead toxicity on dopaminergic neurons, vitamin C plays a critical role in the reversal of lead toxicity ( Musa et al, 2012 ). Other experimental studies have reported comparable results on animals subjected to lead acetate and cadmium chloride ( Kini et al, 2011 ; Ibrahim et al, 2012 ; John et al, 2014 ).…”
Section: Resultsmentioning
confidence: 99%
“…Compared to the control group, prior treatment with vitamin C, when any tested metal was present, avoided the negative influences of heavy metals on the liver's function measures. Through creating inert complexes and reducing lead toxicity on dopaminergic neurons, vitamin C plays a critical role in the reversal of lead toxicity ( Musa et al, 2012 ). Other experimental studies have reported comparable results on animals subjected to lead acetate and cadmium chloride ( Kini et al, 2011 ; Ibrahim et al, 2012 ; John et al, 2014 ).…”
Section: Resultsmentioning
confidence: 99%
“…A recent study corroborates the attenuation of toxicity of early-life (gestational and lactational) Pb exposure in the cerebellum of rat pups upon the supplementation of AA by oral gavage by using the assessments of oxidative stress markers and the antioxidant system, as well as histopathological examinations and tests for neuromotor functions (forelimb grip and negative geotaxis) [ 308 ]. Interestingly, ameliorative effects of AA in Pb poisoning in the cerebellum of adult rats have also been proposed [ 309 ].…”
Section: Aa As a Potential Ameliorative Agent In Pb Neurotoxicitymentioning
confidence: 99%
“…It should be noted that the effect of AA in the restoration of Pb-induced toxicity is not limited to the brain. Indeed, the non-neuronal amelioration of Pb-mediated effects in experimental animals by AA either alone or in combination with other proposed neuroprotective agents has been observed in blood biochemistry and hematological parameters [ 265 , 306 , 307 , 308 , 309 , 310 , 311 , 312 , 313 , 314 , 315 , 316 ], cardiac functions [ 317 ], hepatic physiology [ 277 , 285 , 312 , 318 , 319 , 320 , 321 , 322 , 323 , 324 ], renal functions [ 285 , 310 , 312 , 325 , 326 ], the colon [ 327 ], testicular functions and spermatogenesis [ 285 , 328 , 329 , 330 , 331 , 332 ], sperm morphology and physiology [ 333 ], thyroid hormone synthesis [ 334 ], the lungs [ 335 ], and clastogenicity in bone marrow cells [ 336 , 337 , 338 ]. Readers are suggested to refer to a recent review paper [ 339 ] for a brief overview of the non-neuronal effects of AA in Pb poisoning.…”
Section: Other Non-neuronal Attenuative Effects Of Aa In Pb Poisonmentioning
confidence: 99%