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Neurotoxicol Teratol. 2018 Mar - Apr;66:35-45. doi: 10.1016/j.ntt.2018.01.006. Epub 2018 Jan 17.

Neuroprotective effect of morin on lead acetate- induced apoptosis by preventing cytochrome c translocation via regulation of Bax/Bcl-2 ratio.

Author information

1
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600 113, Tamil Nadu, India. Electronic address: sumathi.doctor@unom.ac.in.
2
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600 113, Tamil Nadu, India.
3
Department of Biotechnology, Rajalakshmi Engineering College, Rajalakshmi Nagar, Thandalam, Chennai 602 105, Tamil Nadu, India.

Abstract

Lead (Pb) intoxication is a prevalent type of environmental toxicity as well as minimal amount of lead exposure is liable for neurobehavioral or perhaps intelligence defects. The present study was undertaken to investigate the beneficial effects of morin in protecting the lead acetate (PbAc)-induced oxidative stress in rat brain. PbAc intoxication resulted in motor deficit, memory impairment and oxidative stress Further, PbAc administration alters Bax/Bcl-2 expression thereby increases cytochrome c release from the mitochondria. Treatment with morin at a dose of 40 mg/kg b.wt. significantly restored back the abnormal changes that were noticed in PbAc intoxicated rats. Histopathological sections of cortex, cerebellum and hippocampus showed the extent of neuronal loss in PbAc induced rats and its restoration upon administration of morin. These outcomes imply that morin might be employed therapeutically to chelate toxic metals like Pb, thus possibly lowering PbAc-induced neurotoxicity and tissue damage.

KEYWORDS:

Apoptosis; Bax; Bcl-2; Cognitive impairment; Cytochrome c; Lead acetate; Morin

PMID:
29353014
DOI:
10.1016/j.ntt.2018.01.006

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