Short-term exposure to benzo[a]pyrene causes oxidative damage and affects haemolymph steroid levels in female crab Portunus trituberculatus

2016 ◽  
Vol 208 ◽  
pp. 486-494 ◽  
Author(s):  
Jianmin Wen ◽  
Luqing Pan
Keyword(s):  
Oxidative Damage ◽  
Portunus Trituberculatus ◽  
Short Term ◽  
Female Crab ◽  
Short Term Exposure

Short-term exposure to formaldehyde promotes oxidative damage and inflammation in the trachea and diaphragm muscle of adult rats

2015 ◽  
Vol 202 ◽  
pp. 45-51 ◽  
Author(s):  
Luiza Fagundes Lima ◽  
Giselle Luciane Murta ◽  
Ana Carla Balthar Bandeira ◽  
Clarissa Rodrigues Nardeli ◽  
Wanderson Geraldo Lima ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Diaphragm Muscle ◽  
Short Term ◽  
Adult Rats ◽  
Short Term Exposure

scholarly journals Curcumin Decreases Hippocampal Neurodegeneration and Nitro-Oxidative Damage to Plasma Proteins and Lipids Caused by Short-Term Exposure to Ozone

Molecules ◽  
2021 ◽  
Vol 26 (13) ◽  
pp. 4075
Author(s):  
María Luisa Mendoza-Magaña ◽  
Hugo Alejandro Espinoza-Gutiérrez ◽  
Sendar Daniel Nery-Flores ◽  
Abraham Alberto Ramírez-Mendoza ◽  
Cesar Ricardo Cortez-Álvarez ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Plasma Lipids ◽  
Biological Activities ◽  
Dietary Supplementation ◽  
Experimental Models ◽  
Male Rats ◽  
Toxic Substances ◽  
Short Term ◽  
Short Term Exposure ◽  
Hippocampal Neurodegeneration

Neurodegeneration is the consequence of harmful events affecting the nervous system that lead to neuronal death. Toxic substances, including air pollutants, are capable of inducing neurodegeneration. Ozone (O3) is the most oxidative toxic pollutant. O3 reacts with cellular components and forms reactive oxygen and nitrogen species, triggering nitro-oxidative damage during short-term exposure. Curcumin (CUR) is a natural phenolic molecule bearing well-documented antioxidant and anti-inflammatory biological activities in diverse experimental models. The aim of this work was to evaluate the effect of preventive dietary administration of CUR against hippocampal neurodegeneration and nitro-oxidative damage caused by short-term exposure to O3. Eighty Wistar male rats were distributed into four experimental groups, twenty rats each: intact control; CUR dietary supplementation without O3 exposure; exposure to 0.7 ppm of O3; and exposed to O3 with CUR dietary supplementation. Five rats from each group were sacrificed at 1, 2, 4, and 8 h of exposure. The CUR dose was 5.6 mg/kg and adjusted according to food consumption. CUR significantly decreased oxidative damage to plasma lipids and proteins, as well as neurodegeneration in CA1 and CA3 hippocampal regions. Concluding, CUR proved effective protection in decreasing neurodegeneration in the hippocampus and prevented systemic oxidative damage.

The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

1976 ◽  
Vol 36 (01) ◽  
pp. 221-229 ◽  
Author(s):  
Charles A. Schiffer ◽  
Caroline L. Whitaker ◽  
Morton Schmukler ◽  
Joseph Aisner ◽  
Steven L. Hilbert
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Dimethyl Sulfoxide ◽  
Platelet Function ◽  
Platelet Volume ◽  
Short Term ◽  
Platelet Factor ◽  
Short Term Exposure ◽  
Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

Short-term exposure and long-term consequences of neonatal exposure to Δ9-tetrahydrocannabinol (THC) and ibuprofen in mice

2016 ◽  
Vol 307 ◽  
pp. 137-144 ◽  
Author(s):  
Gaëtan Philippot ◽  
Fred Nyberg ◽  
Torsten Gordh ◽  
Anders Fredriksson ◽  
Henrik Viberg
Keyword(s):  
Neonatal Exposure ◽  
Short Term ◽  
Short Term Exposure ◽  
Long Term Consequences

scholarly journals Spatio-temporal associations of air pollutant concentrations, GP respiratory consultations and respiratory inhaler prescriptions: a 5-year study of primary care in the borough of Lambeth, South London

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Mark Ashworth ◽  
◽  
Antonis Analitis ◽  
David Whitney ◽  
Evangelia Samoli ◽  
...  
Keyword(s):  
Primary Care ◽  
Negative Binomial ◽  
Hospital Admissions ◽  
Air Pollutant ◽  
Respiratory Morbidity ◽  
Short Term ◽  
Short Term Exposure ◽  
Short And Long Term ◽  
Spatio Temporal

Abstract Background Although the associations of outdoor air pollution exposure with mortality and hospital admissions are well established, few previous studies have reported on primary care clinical and prescribing data. We assessed the associations of short and long-term pollutant exposures with General Practitioner respiratory consultations and inhaler prescriptions. Methods Daily primary care data, for 2009–2013, were obtained from Lambeth DataNet (LDN), an anonymised dataset containing coded data from all patients (1.2 million) registered at general practices in Lambeth, an inner-city south London borough. Counts of respiratory consultations and inhaler prescriptions by day and Lower Super Output Area (LSOA) of residence were constructed. We developed models for predicting daily PM2.5, PM10, NO2 and O3 per LSOA. We used spatio-temporal mixed effects zero inflated negative binomial models to investigate the simultaneous short- and long-term effects of exposure to pollutants on the number of events. Results The mean concentrations of NO2, PM10, PM2.5 and O3 over the study period were 50.7, 21.2, 15.6, and 49.9 μg/m3 respectively, with all pollutants except NO2 having much larger temporal rather than spatial variability. Following short-term exposure increases to PM10, NO2 and PM2.5 the number of consultations and inhaler prescriptions were found to increase, especially for PM10 exposure in children which was associated with increases in daily respiratory consultations of 3.4% and inhaler prescriptions of 0.8%, per PM10 interquartile range (IQR) increase. Associations further increased after adjustment for weekly average exposures, rising to 6.1 and 1.2%, respectively, for weekly average PM10 exposure. In contrast, a short-term increase in O3 exposure was associated with decreased number of respiratory consultations. No association was found between long-term exposures to PM10, PM2.5 and NO2 and number of respiratory consultations. Long-term exposure to NO2 was associated with an increase (8%) in preventer inhaler prescriptions only. Conclusions We found increases in the daily number of GP respiratory consultations and inhaler prescriptions following short-term increases in exposure to NO2, PM10 and PM2.5. These associations are more pronounced in children and persist for at least a week. The association with long term exposure to NO2 and preventer inhaler prescriptions indicates likely increased chronic respiratory morbidity.

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