8.5.1 Metals Affecting Biomineralization
In general, although metallic elements have certain properties in common, each is a
distinct element with its own physicochemical characteristics which determine its
biological or toxicological properties (Duffus 2002). Exposure of cells/organisms
to high levels of nonessential or essential metals causes toxicity which gained
attention of many research groups (ATSDR 2008; Gerber et al. 2002; CICAD
2004; Lima et al. 2008). As an example, manganese (Mn), which at physiological
concentrations is involved in cellular protection, replication and bone mineralization (ATSDR 2008; Santamaria 2008; Daly 2009), can cause toxicity when its
concentration are in excess (Satyanarayana and Saraf 2007).
In sea urchins, toxicity tests on embryos and larvae have been proposed for the
characterization of the effects causes by a variety of toxicants, including essential
and heavy metals. Metals have been classically used as inducers of skeleton
malformations in sea urchin and sea star embryos. These include cadmium (Cd),
zinc (Zn), copper (Cu), chromium (Cr), lead (Pb), nickel (Ni), lithium (Li), manganese (Mn), gadolinium (Gd), whose exposure causes: reduced or absent skeleton,
abnormal branching patterns, extranumerary origin sites were observed (Hardin
et al. 1992; Radenac et al. 2001; Coteur et al. 2003; Russo et al. 2003; Roccheri
et al. 2004; Kobayashi and Okamura 2004; Agca et al. 2009; Kiyomoto et al. 2010;
Pinsino et al. 2010; Saitoh et al. 2010). In some cases, (Cd and Mn exposures)
defects in biomineralization have been correlated to the expression of stress
proteins, such as hsp60 and hsp70 (Roccheri et al. 2004; Pinsino et al. 2010),
apoptosis (Filosto et al. 2008), and Metallothionein mRNA overexpression
(Russo et al. 2003). The expression of biomineralization-related genes has been
investigated only in lithium-treated and in zinc-treated embryos, by a high throughput analysis based on gene array screening and whole mount in situ hybridization,
providing evidence of the differential expression of more than 4,000 and 250 genes,
respectively (Poustka et al. 2007). Four genes expressed in PMCs, namely, Pmar,
SMAD2, P19, SM50, seemed to be lightly upregulated upon treatment. Further
investigation is needed in this direction.
8.5.2 Ionizing Radiations
An increase in UV-B radiation due to the thinning of the ozone hole can reach the
Earth, including marine ecosystems. Although the penetration of UV-B into natural
waters can vary, depending on the concentration and optical qualities of dissolved
organic matter, phytoplankton, or other suspended particles (Dunne and Brown
1996), its consequences can have serious effects on organisms. Some planktonic
embryos, larvae, and adults of many species are more prone to UV-B as they dwell
in the top layers of the water column (Hader 2000). Harmful effects of waterpenetrating UV-B radiation cause strong impairment of development as well as
modifications in cellular protein composition, especially in the modulation of stress
240
V. Matranga et al.
In general, although metallic elements have certain properties in common, each is a
distinct element with its own physicochemical characteristics which determine its
biological or toxicological properties (Duffus 2002). Exposure of cells/organisms
to high levels of nonessential or essential metals causes toxicity which gained
attention of many research groups (ATSDR 2008; Gerber et al. 2002; CICAD
2004; Lima et al. 2008). As an example, manganese (Mn), which at physiological
concentrations is involved in cellular protection, replication and bone mineralization (ATSDR 2008; Santamaria 2008; Daly 2009), can cause toxicity when its
concentration are in excess (Satyanarayana and Saraf 2007).
In sea urchins, toxicity tests on embryos and larvae have been proposed for the
characterization of the effects causes by a variety of toxicants, including essential
and heavy metals. Metals have been classically used as inducers of skeleton
malformations in sea urchin and sea star embryos. These include cadmium (Cd),
zinc (Zn), copper (Cu), chromium (Cr), lead (Pb), nickel (Ni), lithium (Li), manganese (Mn), gadolinium (Gd), whose exposure causes: reduced or absent skeleton,
abnormal branching patterns, extranumerary origin sites were observed (Hardin
et al. 1992; Radenac et al. 2001; Coteur et al. 2003; Russo et al. 2003; Roccheri
et al. 2004; Kobayashi and Okamura 2004; Agca et al. 2009; Kiyomoto et al. 2010;
Pinsino et al. 2010; Saitoh et al. 2010). In some cases, (Cd and Mn exposures)
defects in biomineralization have been correlated to the expression of stress
proteins, such as hsp60 and hsp70 (Roccheri et al. 2004; Pinsino et al. 2010),
apoptosis (Filosto et al. 2008), and Metallothionein mRNA overexpression
(Russo et al. 2003). The expression of biomineralization-related genes has been
investigated only in lithium-treated and in zinc-treated embryos, by a high throughput analysis based on gene array screening and whole mount in situ hybridization,
providing evidence of the differential expression of more than 4,000 and 250 genes,
respectively (Poustka et al. 2007). Four genes expressed in PMCs, namely, Pmar,
SMAD2, P19, SM50, seemed to be lightly upregulated upon treatment. Further
investigation is needed in this direction.
8.5.2 Ionizing Radiations
An increase in UV-B radiation due to the thinning of the ozone hole can reach the
Earth, including marine ecosystems. Although the penetration of UV-B into natural
waters can vary, depending on the concentration and optical qualities of dissolved
organic matter, phytoplankton, or other suspended particles (Dunne and Brown
1996), its consequences can have serious effects on organisms. Some planktonic
embryos, larvae, and adults of many species are more prone to UV-B as they dwell
in the top layers of the water column (Hader 2000). Harmful effects of waterpenetrating UV-B radiation cause strong impairment of development as well as
modifications in cellular protein composition, especially in the modulation of stress
240
V. Matranga et al.