Abstract
Lead poisoning is one of the most significant health problem of environmental origin. It is known to cause different damages in the central and peripheral nervous system which could be represented by several neurophysiological and behavioral symptoms. In this study we firstly investigated the effect of lead prenatal exposure in rats to (3g/L), from neonatal to young age, on the motor/sensory performances, excitability of the spinal cord and gaits during development. Then we evaluated neuroprotective effects of curcumin I (Cur I) against lead neurotoxicity, by means of grasping and cliff avoidance tests to reveal the impairment of the sensorimotor functions in neonatal rats exposed prenatally to lead. In addition, extracellular recordings of motor output in spinal cord revealed an hyper-excitability of spinal networks in lead treated rats. The frequency of induced fictive locomotion was also increased in treated rats. At the young age, rats exhibited an impaired locomotor gait. All those abnormalities were attenuated by Cur I treatment at a dose of 16g/kg. Based on our finding, Cur I has shown features of a potent chemical compound able to restore the neuronal and the relative locomotor behaviors disturbances induced by lead intoxication. Therefore, this chemical can be recommended as a new therapeutic trial against lead induced neurotoxicity.
Highlights
Lead (Pb) an ubiquitous environmental pollutant [1], causes lead poisonning that remains an important pediatric health problem in both developed and developing countries [2]
Prenatal lead exposure induced weight loss in pups and curcumin I (Cur I) gain it Our data have shown that Pb intoxication (3g/L) reduces significantly (p = 0.004; 0.002; 0.003; 0.004) the pups body weight in comparison to controls, for all ages (P1(5.28±0.22 vs 7.482 ± 0.12), P2 (6.09 ± 0.16 vs 8.07 ± 0.18) (Fig 1A), (P22 (38±3.79 vs 54.57 ± 2.36), P40 (137.4 ± 3.93 vs 170.5 ± 9.63) except for P60 in which the body weight loss is not significant (0.083) (Fig 1B)
Treatment with Cur I (16g/Kg) seems to restore the body weight deficiency of the intoxicated group at all developmental stages but more significantly for the young ages compared to Pb group (P1 (7.26 ± 0.17 vs 5.28 ± 0.22), P2 (7.37 ± 0.13 vs 8.07 ± 0.18), P22 (54.8 ± 1.77 vs 38±3.79)) (p = 0.001; 0.004; 0.006)
Summary
Lead (Pb) an ubiquitous environmental pollutant [1], causes lead poisonning that remains an important pediatric health problem in both developed and developing countries [2]. Genetic, metabolic, and enzymatic damages [3] and causes well documented hematological and gastrointestinal dysfunctions as well as the production of neurological impairments. Pb exposure affects a variety of neurotransmitter systems resulting in a wide range of adverse effects, in the developing brain and spinal cord [9, 10]. Several studies indicate that Pb affects the monoaminergic system activity during development of adult’s central nervous system (CNS) [10,11,12] and alters glutamate and GABA-ergic systems [13, 14]
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