Effects of Continuous Low-Dose Exposure to Organic and Inorganic Mercury During Development on Epileptogenicity in Rats

Preventive Effect of CuCl2on Behavioral Alterations and Mercury Accumulation in Central Nervous System Induced by HgCl2in Newborn Rats

“…Studies have reported that the exposure to HgCl 2 is able to induce behavioral alterations during brain developmental periods and, more recently, in adult rats . In the present study, utilizing the two behavioral tests, we verified that the motor function, muscular strength and size, and cerebellar function were damaged in young rats exposed to Hg.…”

Methylmercury: A potential environmental risk factor contributing to epileptogenesis

“…Electrocorticographic examinations showed a significant increase in the frequency and summated duration of paroxysmal activity and probability of generalized seizures in MeHg-treated animals at both postnatal day 28 (PND28) and PND90; epileptic activity spread over the whole cortical surface of the brains. These data suggest that pre- and postnatal MeHg exposure significantly increased the susceptibility of both young and adult animals to seizures and facilitated propagation of epileptiform activity (Szász et al, 1999, 2002). Similar effects were also seen in the offspring of rats that were exposed to inorganic mercury (Hg 2+ ) under similar experimental conditions, although the effect of Hg 2+ on epileptogenicity appeared to be long-lasting (Szász et al, 2002).…”

“…These data suggest that pre- and postnatal MeHg exposure significantly increased the susceptibility of both young and adult animals to seizures and facilitated propagation of epileptiform activity (Szász et al, 1999, 2002). Similar effects were also seen in the offspring of rats that were exposed to inorganic mercury (Hg 2+ ) under similar experimental conditions, although the effect of Hg 2+ on epileptogenicity appeared to be long-lasting (Szász et al, 2002). In agreement with these findings, prenatal and postnatal exposure of rats to MeHg using the same exposure paradigm as described above resulted in a decreased threshold for evoking excitatory postsynaptic potentials and spikes in neurons of neocortical slices, suggesting an increase in neuronal excitability (Világi et al, 2000).…”

“…Szász et al (1999, 2002) showed that exposure of rats to low levels of MeHg (0.375 mg/kg body weight/day) during the entire mating, gestation and lactation period significantly enhanced epileptogenicity in their offspring compared with those of age-matched controls in response to chemoconvulsive agent 3- or 4-aminopyridine. Electrocorticographic examinations showed a significant increase in the frequency and summated duration of paroxysmal activity and probability of generalized seizures in MeHg-treated animals at both postnatal day 28 (PND28) and PND90; epileptic activity spread over the whole cortical surface of the brains.…”

Characterization of methylmercury demethylation in the central nervous system.

“…The primary mechanism by which mercury, both inorganic (iHg) and organic (MeHg), exerts its toxic effects is through the binding of sulfhydryl groups on protein residues which may lead to altered protein function (2005b; Cabanero et al, 2005;Costa et al, 2004;Fitsanakis & Aschner, 2005;Gailer et al, 2000;Szasz et al, 2002). The manifestation of Hg toxicity is likely due to secondary effects including alterations of calcium homeostasis (Limke et al, 2004), and generation of reactive oxygen species (ROS) (Dreiem et al, 2005;Chapman & Chan, 1999;Allen et al, 2002); which ultimately lead to cell death and other toxic responses.…”