Cytogenetic, developmental, and biochemical effects of aluminum, iron, and their mixture in sea urchins and mussels

Abstract

The present study was undertaken to evaluate the toxicity of aluminum sulfate, ferric chloride and their 1:1 mixture (Mix) on early development, fertilization and offspring quality in three sea urchins species (Sphaerechinus granularis, Paracentrotus lividus, Psammechinus microtuberculatus) and in mussels (Mytilus galloprovincialis). The endpoints were the following: a) larval malformations; b) developmental arrest; c) embryonic mortality; d) fertilization success; e) cytogenetic effects, and f) luminol-dependent chemiluminescence (LDCL). Overall data point to the induction of developmental defects in both sea urchin and mussel embryos following exposure of embryos to Al(III) or Fe(III) (10(-7) to 10(-6) M), whereas Mix caused varied effects vs. Al(III) or Fe(III) alone, from scarce or no additive effects (M. galloprovincialis and P. lividus) to a dramatic rise in embryolethality even at nominal levels of 10(-8) M (Ps. microtuberculatus).S. granularis sperm underwent a dose-dependent decrease in fertilization success following exposure to Al(III), or Fe(III), or Mix at levels ranging from 10(-8) to 10(-5) M. A significant increase of developmental defects was observed in the offspring of S. granularis sperm exposed to micromolar levels of the agents, suggesting an Al(III)- and Fe(III)-related transmissible damage to sperm. The cytogenetic analysis of Al(III)-, Fe(III)-, or Mix-exposed S. granularis embryos showed a significant increase in mitotic aberrations. A relevant feature of the observed cytogenetic damage included scattered chromosomes, suggesting cytoskeleton damage. The LDCL emission in S. granularis embryos showed a dose-related inhibition by agent levels ranging from 10(-7) to 10(-5) M; this held true for both spontaneous and, to a larger extent, for horseradish peroxidase (HRP)-activated LDCL. LDCL associated with fertilization was affected by Al(III), Fe(III) and Mix, with a time- and dose-related shift from stimulation to inhibition. The changes observed in LDCL emission suggested that the observed damage to embryogenesis, fertilization and mitotic activity may be related, at least partly, to alterations of the embryo prooxidant state. The present data point to developmental, cytogenetic and biochemical changes related to realistic levels of Al(III), Fe(III) and their mixtures, raising concern as to their environmental, occupational and iatrogenic exposures.

Toxicity reduction in leather tanning wastewater by improved coagulation flocculation process

“…In that period, raw (R), coagulated (CF), biological effluent (B) wastewater samples and the conditioned sludge (CS) taken from the CODISO showed a toxicity ranking of effluents as CS > CF ≥ R >> B on sea urchins and marine micro algae for the wastewater characteristics given in Table 3 [12]. The toxicity in CF sample was attributed to the residual Al(III) and Fe(III) considering the previous findings [25,26]. Figure 1 shows the immobilization D. magna exposed to the coagulated effluents at different dilutions.…”

Chemical speciation and toxicity of metals assessed by three bioluminescence‐based assays using marine organisms

“…These metals are also known to affect sea urchin fertilization and embryonic development at comparable concentrations (Kennish, 1997). The elements Cr, Zn, Al, and Fe inhibit sea urchin embryonic development (Pagano et al, 1996;Kennish, 1997) at concentrations that had no effect on photocytes. As the echinoderm embryonic development bioassay belongs to the noncatalytic group of toxicity assays, the photocyte-embryonic development toxicity discrepancy does not necessarily indicate the photocyte bioassay is the least sensitive; rather, it implies a difference in sensitivity for those metals between the pre-and post-metamorphic stages of development in echinoderms.…”

L‐Methionine Induces Stage‐Dependent Changes of Differentiation and Oxidative Activity in Sea Urchin Embryogenesis

“…In a previous study, we have observed that allopurinol exerted developmental toxicity only to sea urchin embryos exposed in early developmental stages (before hatching), whereas post-hatching exposures were ineffective (Graillet et al 1993). More recently, we have reported that aluminium and iron(II1) salts both induce developmental and cytogenetic damage, and modulate reactive oxygen species formation at fertilisation and in embryogenesis (Pagano et al 1996).…”

“…1989;Gomez et al 1991;Pagano et al 1996). On the other hand, also a decrease in reactive oxygen species formation has been related to defects in embryogenesis or cell differentiation, as developing embryos or differentiating cells are affected by hypoxia or antioxidants (Allen et al 1985;Allen & Venkatraj 1992;Hansberg et al 1993).…”