Cadmium induces an apoptotic response in sea urchin embryos

Abstract

Cadmium is a heavy metal toxic for living organisms even at low concentrations. It does not have any biological role, and since it is a permanent metal ion, it is accumulated by many organisms. In the present paper we have studied the apoptotic effects of continuous exposure to subacute/sublethal cadmium concentrations on a model system: Paracentrotus lividus embryos. We demonstrated, by atomic absorption spectrometry, that the intracellular amount of metal increased during exposure time. We found, using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, that long treatments with cadmium triggered a severe DNA fragmentation. We demonstrated, by immunocytochemistry on whole-mount embryos, that treatment with cadmium causes activation of caspase-3 and cleavage of death substrates ␣-fodrin and lamin A. Incubating the embryos since fertilization with Z-DEVD FMK, a caspase-3 inhibitor, we found, by immunocytochemistry, that cleavage by caspase-3 and cleavage of death substrates were inactivated.

Autophagy as a defense strategy against stress: focus on Paracentrotus lividus sea urchin embryos exposed to cadmium

“…In contrast, if the Cd insult is much higher (i.e., 1 mM lasting 24 h), the killed cells are more numerous and, after the Cd removal, the normal development cannot be restored (Roccheri et al 2004;Agnello et al 2007). A further study showed for the first time the induction of autophagy that displays a maximum peak after 18 h of Cd exposure, when apoptosis is just beginning.…”

“…These researches indicated that the exposure of the developing embryo to subacute/sublethal concentrations of Cd induce, firstly, the activation of the early defense mechanisms, such as the synthesis of HSPs and metallothioneins (Russo et al 2003;Roccheri et al 2004), but if this is not sufficient to safeguard the developmental program, embryos will trigger the autophagic and/or apoptotic processes (Chiarelli et al 2011;Agnello et al 2007). Some of the pathways activated in sea urchin P. lividus embryos, showed in Table 1, can be occur in tandem or in sequence.…”

Manganese: A New Emerging Contaminant in the Environment

“…The authors found that 9 hours of cadmium exposure were required to induce the synthesis of HSPs 70 and 72, while at least 15 hours were needed to observe the induction of hsp56 and 25kDa synthesis. In addition, it has been demonstrated that a long-lasting exposure (over 24 hours) triggers DNA fragmentation and causes the activation of caspase-3, one of the key molecules promoting apoptosis, which increased in a time-dependent way (Agnello et al 2006(Agnello et al , 2007. In sea urchin embryos, apoptosis is an important part of the defence strategy, both in physiological or stress conditions (Agnello & Roccheri, 2010).…”

Introductory Chapter: Sea Urchin - Knowledge and Perspectives

“…A xenobiotic able to cause a strong activation of all embryonic defence mechanisms reported in (Figure 3) is cadmium, an heavy metal [47,[50][51][52][53]. It must be underlined that such defence mechanisms are basally activated in physiological conditions and that their extent highly increases in stress conditions.…”