Effects of a municipal effluent on the freshwater mussel Elliptio complanata following challenge with Vibrio anguillarum

The purpose of this study was to examine the cumulative effects of exposure to a pathogenic bacteria and municipal effluent in the freshwater mussel Elliptio complanata. Mussels were exposed to increasing concentrations of an ozone-treated effluent at 15°C for 7 days. A sub-group of mussels was inoculated with Vibrio anguillarum and exposed to the same conditions as above.After the exposure period, mussels were collected to assess hemocyte count and viability,immunocompetence(phagocytosis and nitrite production), oxidative stress/inflammation(cyclooxygenase and lipid peroxidation) and oxygen radical/xenobiotic scavenging activity(metallothioniens, glutathione S-transferase). The results showed that mussels exposed to municipal effluent had increased hemocyte counts, phagocytosis, nitrites, lipid peroxidation and metallothioneins. In the inoculated mussels, the same responses were observed, in addition to cyclooxygenase and glutathione S-transferase activities. Multivariate analyses revealed that(1)the response pattern changed with effluent concentration, where increased responses observed at low effluent concentrations(10%, V/V) were attenuated at higher effluent concentrations,(2)the effluent produced more pronounced changes in lipid peroxidation, metallothionein and hemocyte viability, and(3) the simultaneous presence of V. anguillarum led to more important changes in hemocyte count and viability and nitrite levels. In conclusion, the presence of V.anguillarum could alter the response of mussels to municipal effluent, which could lead to increased inflammation in mussels.     

Oxidative stress, endothelial dysfunction and inflammatory response in rat heart to NO₂ inhalation exposure

Epidemiological studies suggest that NO₂ inhalation is associated with adverse effects on heart-related health, however, existing experimental data lack relevant evidences. In this study, a role for oxidative stress, endothelial dysfunction and inflammatory responses in the heart of rats treated with different concentrations of NO₂ (0, 5, 10 and 20 mg m⁻³) was investigated. Mild heart pathology occurred after 7-d exposure (6 h d⁻¹). Marked oxidative stress were induced as evaluated by reduction/induction of antioxidants (Cu/Zn-SOD, Mn-SOD and GPx) activity and increasing formation of MDA and PCO. Also, mRNA and protein biomarkers of vasoconstriction (ET-1, eNOS) and inflammation (TNF-α, IL-1β and ICAM-1) were up-regulated, and p53 mRNA expression, bax/bcl-2 ratio and the mean number of TUNEL-positive myocytes were increased as well. All the results implicate that NO₂ exerted injuries to mammals’ heart, and the damage mechanisms were possibly associated with oxidative stress, endothelial dysfunction and inflammation.