Hippocampal acetylcholinesterase activation induced by streptozotocin in mice is protected by an organotellurium compound without evidence of toxicity.

The cognitive deficit, which is like Alzheimer's disease and is associated with oxidative damage, may be induced by exposure to streptozotocin. This study aimed to evaluate if the tellurium-containing organocompound, 3j, 5'-arylchalcogeno-3-aminothymidine derivative, interferes with the effects of streptozotocin, as well as to investigate its toxicity in adult mice. Cognitive deficit was induced by two doses of streptozotocin (2.25 mg/kg/day, 48 h interval) intracerebroventricularly. After, the mice were subcutaneously treated with 3j (8.62 mg/kg/day) for 25 days. The effects were assessed by evaluating hippocampal and cortical acetylcholinesterase and behavioral tasks. 3j toxicity was investigated for 10 (0, 21.55, or 43.10 mg/kg/day) and 37 (0, 4.31, or 8.62 mg/kg/day) days by assessing biometric parameters and glucose and urea levels, and alanine aminotransferase activity in blood plasma. 3j exposure did not alter the behavioral alterations induced by streptozotocin exposure. On the other hand, 3j exposure normalized hippocampus acetylcholinesterase activity, which is enhanced by streptozotocin exposure. Toxicity evaluation showed that the administration of 3j for either 10 or 37 days did not cause harmful effects on the biometric and biochemical parameters analyzed. Therefore, 3j does not present any apparent toxicity and reverts acetylcholinesterase activity increase induced by streptozotocin in young adult mice.

Behavioral alterations induced by HgCl2 depend on the postnatal period of exposure.

This paper shows the toxicity of mercury (HgCl(2) 5mg/kg/day for 5 days, sc) applied at specific stages of development (1-5, 8-12 or 17-21 days old, 1st, 2nd and 3rd phases, respectively) on the performance of rats in three behavioral tasks and on cerebral mercury levels. The mercury exposure at the 1st and 2nd phases affected the performances of rats in the rim escape. Spontaneous alternation behavior was not altered by mercury exposure. In the open field task, habituation was absent when the rats were treated at the 1st phase, and the crossing response number was lower in rats exposed to mercury at the last period. In general, the brain accumulated large quantities of mercury. In short, the first days of postnatal life (1st phase) appeared to be more sensitive to mercury exposure than the other phases studied, since they presented behavioral deficits even at a time period somewhat after the exposure.

Effects of zinc and cadmium on HgCl2-delta-ALA-D inhibition and Hg levels in tissues of suckling rats.

The effects of CdCl2 and ZnCl2 pretreatments on the inhibition of delta-ALA-D (delta-aminolevulinic acid dehydratase) activity and Hg contents in liver and kidneys of suckling rats intoxicated with HgCl2 were investigated. Zn-pretreatment prevented the effects of mercury at a higher magnitude than CdCl2. Hepatic and renal delta-ALA-D activities were significantly inhibited by HgCl2 and prior exposure to CdCl2 partially prevented the renal effect of mercury but not altered the mercury levels in both tissues. Pretreatment with ZnCl2 abolished mercury-induced delta-ALA-D-inhibition in kidneys and liver and induced an increase in renal (about three times) and a decrease in hepatic (to one-third) Hg contents when compared to the group injected only with mercury. In face of zinc effects to prevent Hg-delta-ALA-D inhibition and to alter Hg-deposition levels in kidney and liver, these results suggest that these effects may be partially due to the synthesis of metallothioneins (MT). In fact, liver MT content presented by animals pretreated with zinc was significantly greater than control and Hg-treated groups, but the increase showed by renal tissue (about 60%) was not significant. Although the MT is rich in cysteine (-SH) and consequently can form a great number of MT-Hg complex, other mechanisms should be also involved in zinc protection on mercury toxicity.