Influences of Cu or Cd on the neurotoxicity induced by petroleum hydrocarbons in ragworm Perinereis aibuhitensis

The ecotoxicological effects of heavy metals and petroleum hydrocarbons （PHCs） on ragworms are still vague. The relationships between toxicological indices （mortality and acetylcholinesterase （ACHE） activity） and concentrations of toxicants （Cu, Cd, and PHCs） were examined in the estuary keystone species Perinereis aibuhitensis in laboratory conditions. The results of single toxicant indicated that three toxicants had potentially physiological toxicity to P. aibuhitensis. The estimated 4-d and 10-d LC50 for Cu, Cd, and PHCs was derived from the relationships between mortality and toxicants concentrations. Notable changes in the morphological signs and symptoms of P. aibuhitensis exposed to PHCs were observed. The ACHE activity of P. aibuhitensis was more sensitive to the toxicity of PHCs than the others. The results of combined toxicants implied that the combined toxicity of Cu or Cd and PHCs to P. aibuhitensis was related to the concentration combination of toxicants. Compared to single PHCs treatment, the addition of Cu or Cd significantly mitigated the neurotoxicity of PHCs to ACHE activity in P. aibuhitensis, which showed an antagonistic effect.

Study on Insecticidal Activities and Effect on Three Kinds of Enzymes by 5-Aminolevulinic Acid on Oxya chinensis

Insecticidal activities and effects on three enzymic activities caused by 5-aminolevulinic acid （ALA） on Oxya chinensis were studied. Fourth-instar nymphs of O. chinensis were treated with different doses ofALA （A1,250 mM; A2, 450 mM; A3,750 mM; A4, 1 000 mM）. Mortality and the activities of acetylcholinesterase （ACHE）, glutathione S-transferase （GSTs）, and glutathione peroxidase （GPx） were determinated. The mortality of O. chinensis rose with an increasing dose of ALA. The mortality of high-dose treatments A3 and A4 reached 66.19 and 80.21%, respectively. The value of LD50 was 3.61 （3.29-3.93） mg·g^-1 body weight （95% confidence interval）. Biochemical studies showed that the activities of AChE and GPx in the A4 treatment declined by 51.53 and 42.82% in the female, and 42.65 and 43.85% in the male compared to the control, respectively, and the degree of decline reached a significant level at P 〈 0.05. Meanwhile, the GSTs activities of O. chinensis enhanced with increasing dose of ALA. The GSTs activities of female and male O. chinensis in the A4 treatment remarkably increased by 171.05 and 97.42% compared to the control （P〈 0.05）. ALA had an obviously toxic effect on O. chinensis. Moreover, ALA caused the photoinactivation of AChE and GPx, which induced nerve transmission blocking and the capability to defend oxidation damage declining. Meanwhile, a high dose of ALA could activate GSTs, which caused a feedback inhibition of the insect to the phototoxic substance.

Dioxin induces expression of hsa-mi R-146b-5p in human neuroblastoma cells

Dioxin can cause a series of neural toxicological effects. Micro RNAs（mi Rs） play important roles in regulating nervous system function and mediating cellular responses to environmental pollutants, such as dioxin. Hsa-mi R-146 b-5 p appears to be involved in neurodegenerative diseases and brain tumors. However, little is known about effects of dioxin on the expression of hsa-mi R-146 b-5 p. We found that the hsa-mi R-146 b-5 p expression and its promoter activity were significantly increased in dioxin treated SK-N-SH cells, a human-derived neuroblastoma cell line. Potential roles of hsa-mi R-146 b-5 p in mediating neural toxicological effects of dioxin may be due to the regulation of certain target genes. We further confirmed that hsa-mi R-146 b-5 p significantly suppressed acetylcholinesterase（ACh E） activity and targeted the3′-untranslated region of the ACh E T subunit, which has been down-regulated in dioxin treated SK-N-SH cells. Functional bioinformatic analysis showed that the known and predicted target genes of hsa-mi R-146 b-5 p were involved in some brain functions or cyto-toxicities related to known dioxin effects, including synapse transmission, in which ACh E may serve as a responsive gene for mediating the effect.