Prevention of cadmium‑induced neurotoxicity in rats by essential nutrients present in nuts


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.
Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 International License.

Copyright (c) 2019 Acta Neurobiologiae Experimentalis


Download data is not yet available.