Individual and joint toxic effects of cadmium sulfate and α-naphthoflavone on the development of zebrafish embryo

Abstract

This paper aims to evaluate the individual and joint toxicities of cadmium sulfate (CdSO4) and α-naphthoflavone (ANF) in zebrafish embryos. As a result, CdSO4 caused both lethal and sub-lethal effects, such as 24 h post-fertilization (hpf) death and 72 hpf delayed hatching. However, ANF only caused sub-lethal effects, including 48 hpf cardiac edema and 72 hpf delayed hatching. Taking 24 hpf death and 48 hpf cardiac edema as endpoints, the toxicities of CdSO4 and ANF were significantly enhanced by each other. Consistently, both CdSO4 and ANF caused significant oxidative stress, including decreases in the reduced glutathione (GSH) level, inhibition of superoxide dismutase (SOD) activity, as well as increases in malondialdehyde (MDA) content in zebrafish embryos, but these mixtures produced much more significant alterations on the biomarkers. Co-treatment of CdSO4 and ANF significantly down-regulated the mRNA level of multidrug resistance-associated protein (mrp) 1 and cytochrome P450 (cyp) 1a, which constituted the protective mechanisms for zebrafish embryos to chemical toxins. In conclusion, co-treatment of CdSO4 and ANF exhibited a much more severe damage in zebrafish embryos than individual treatment. Meanwhile, production of oxidative stress and altered expression of mrp1 and cyp1a could be important components of such joint toxicity.

The role of Nrf1 and Nrf2 in the regulation of glutathione and redox dynamics in the developing zebrafish embryo

“…GSSG was also increased by tBOOH treatment in control embryos, and increased slightly in Nrf2a and Nrf2b morphants by tBOOH treatment. Cells have the ability to export GSSG [40] , [41] , and these exporters were measured in the embryo [42] , [43] . In this study, we only examined the response to pro-oxidant challenge 2 h after initial tBOOH exposure, allowing for potential recovery.…”

Glutathione and zebrafish: Old assays to address a current issue

“…Typically upon induction of oxidative stress, the concentration of GSH decreases. GSH concentration in zebrafish has been shown to decrease in response to arsenic, atrazine (Adeyemi et al, 2015), cadmium, chromium (Jin et al, 2015a), cadmium sulfate, α-naphthoflavone (Yin et al, 2014), chlorpyrifos (Jin et al, 2015b), PCB 126 (Liu et al, 2015), silver nanoparticles (Massarsky et al, 2013), titanium dioxide nanoparticles (Faria et al, 2014), bisphenol A, nonylphenol (Wu et al, 2011), selenomethionine (Arnold et al, 2016), and ion radiation (Si et al, 2013). The decrease in GSH supports its utilization to neutralize ROS; however, not all exposures result in GSH decrease.…”

“…GSH and GSSG concentrations can also be evaluated using commercially available kits from Cayman Chemical Company (Ann Arbor, MI) as in Jaja-Chimedza et al (2012), Beyotime Institute of Biotechnology (Nantong, China) as in Yin et al (2014), as well as Nanjing Jiancheng Bioengineering Institute (Nanjing, China) as in Jin et al (2015a), Jin et al (2015b), Liu et al (2015), Si et al (2013), Wu et al (2011), and Yang et al (2014). Several kits are also available through Sigma-Aldrich (St. Louis, MO); however, to the best of our knowledge, these are yet to be used with zebrafish.…”

Regulation of Human Cytochrome P4501A1 (hCYP1A1): A Plausible Target for Chemoprevention?

“…Treatment with the CYP1A inhibitor, α -naphthoflavone, shows that the activity of CYP1A1 is important for the proper development of the embryo's cardiovascular system [141–143]. However, so far there is not enough information about the impact of this isoform in the endogenous metabolism, so it is essential to conduct more studies that can help us to understand the mechanisms of these processes and their impact on the human health.…”