Trans-generational effects of copper on nerve damage in Caenorhabditis elegans

Abstract

The potential toxicity of copper has received great attention for a long time, however, trans-generational effects of copper have not been extensively investigated. Caenorhabditis elegans (C. elegans) was used to evaluate the trans-generational toxicities of copper several physiological endpoints: growth, head thrashes and body bends and degree of neuronal damage. Copper significantly inhibited growth, body bends, head thrashes and caused degeneration of dopaminergic neurons in a concentration-dependent manner in parental worms. Further we found oxidative damage was to underlying the onset of neuron degeneration. In our study copper promoted ROS accumulation, and led to an increased expression of the oxidative stress response-related genes sod-3 and a decreased expression of metal detoxification genes mtl-1 and mtl-2. Moreover, copper increased the fluorescence intensity of the transgenic strain that encodes the antioxidant enzyme SOD-3. Gradually decline in copper-induced impairments were observed in the filial generations without exposure. No growth impairment was shown in F3, the trend of head thrashes recovery gradually appeared in F2 and no growth impairment was shown in F3, the body bends impairment caused by the parental copper exposure was recovery until F4 and no growth impairment was shown in F5. Besides, dopamine neurons revealed damage related to neurobehavioral endpoints, with hereditary effects in the progeny together. In addition, sequencing results suggested that copper exposure could cause epigenetic changes. QRT-PCR results showed that differentially expressed genes can also be passed on to offspring.