Contributions of altered permeability of intestinal barrier and defecation behavior to toxicity formation from graphene oxide in nematode Caenorhabditis elegans

Abstract

Graphene oxide (GO) has been extensively studied for potential biomedical applications. Meanwhile, potential GO toxicity arises in both biomedical applications and non-biomedical products where environmental exposures may occur. In the present study, we examined the potential adverse effects of GO and the underlying mechanism using nematode Caenorhabditis elegans as the assay system. We compared the in vivo effects of GO between acute exposure and prolonged exposure, and found that prolonged exposure to 0.5-100 mg L(-1) of GO caused damage on functions of both primary (intestine) and secondary (neuron and reproductive organ) targeted organs. In the intestine, ROS production was significantly correlated with the formation of adverse effects on functions of both primary and secondary targeted organs. GO could be translocated into intestinal cells with loss of microvilli, and distributed to be adjacent to or surrounding mitochondria. Prolonged exposure to GO resulted in a hyper-permeable state of the intestinal barrier, an increase in mean defecation cycle length, and alteration of genes required for intestinal development and defecation behavior. Thus, our data suggest that prolonged exposure to GO may cause potential risk to environmental organisms after release into the environment. GO toxicity may be due to the combinational effects of oxidative stress in the intestinal barrier, enhanced permeability of the biological barrier, and suppressed defecation behavior in C. elegans.

Adverse effects of coal combustion related fine particulate matter (PM 2.5 ) on nematode Caenorhabditis elegans

“…The method for intestinal autofluorescence was performed as described previously (Wu et al, 2013b. Intestinal autofluorescence caused by lysosomal deposits of lipofuscin can accumulate over time in aging nematodes or nematodes exposed to specific toxicants Wu et al, 2013b).…”

Toxicity evaluation of boron nitride nanospheres and water-soluble boron nitride in <em>Caenorhabditis elegans</em>

“…Given that ROS production indicates the toxicity of nanobiomaterials, eg, GO, 28 CNTs, 26 TiO 2 , and ZnO, 36,40 our data here suggest that ROS overproduction in the intestine tissue might be one of the mechanisms underlying adverse BNNS and BN-800-2 effects.…”

“…[19][20][21] These NMs include metal nanoparticles (NPs; TiO 2 , Al 2 O 3 , and ZnO 2 ) [22][23][24] and carbon NPs (carbon NTs [CNTs], graphene oxide [GO], and graphite nanoplatelets). [25][26][27][28] Here, we analyze the two aforementioned representative forms of BN NMs in C. elegans: BNNSs and BN-800-2. In this study, we examined the multiple phenotypic toxicities of two types of BN NMs with different morphology, size, and solubility using C. elegans in aqueous media.…”

“…These results indicate that BN-800-2 more prevalently affected the expression of ROS-related genes than BNNSs, suggesting BN-800-2 might induce more severe oxidative damage. Similarly, other ENM exposure also led to changed expression levels in oxidation-related genes, such as upregulation of SOD2, SOD3, ISP1, GAS1, and CLK1 for CNT exposure, 42 upregulation of SOD1, SOD2, SOD3, ISP1, and CLK1 for GO exposure, 28 and upregulation of HSP16.1, HSP70, SOD1, SOD2, SOD3, and CTL2 for ZnO NP exposure. 40 …”

The Toxicity Assessment of ethyl p-hydroxybenzoate in Nematode C. elegans

“…Neuron may be important secondary targeted organs for toxicants in nematodes ) (Wu, Yin, Li, Tang & Wang, 2013). we evaluated the possibly toxic effects of EP exposure on the locomotion behavior of nematodes．Head thrashes and body bends were used to assay the locomotion behavior of C elegans (Roh & Choi ,2008)． Prolonged exposure to 100 μg/ml of EP did not significantly influence locomotion behavior(head thrashes and body bends) of nematodes.…”