The influence of hyperbaric oxygen therapy on intestinal mucosal barrier function in rats with acute carbon monoxide poisoning

Hyperbaric oxygen increases the partial pressure of O₂ in arterial blood and tissues and thereby relieves cellular hypoxia. We investigated whether this treatment changes biochemical parameters and intestinal mucosal barrier function in rats exposed to toxic levels of CO. Groups of ten Sprague–Dawley rats were treated with CO, with hyperbaric oxygen, or with CO followed by hyperbaric oxygen. A fourth group maintained under normal atmospheric conditions served as a control. CO poisoning increased red blood cell distribution width and the amount of alanine aminotransferase, urea nitrogen, and tight junction creatine kinase but decreased the mean corpuscular hemoglobin (Hb). These changes were reversed after hyperbaric oxygen therapy, which increased the number of red blood cells, hematocrit level, total protein, and Hb level. Hyperbaric oxygen therapy also increased tight junction protein 1 expression and reduced toll-like receptor 4 expression in the rat colon. In conclusion, hyperbaric oxygen resulted in an improved oxic condition in CO-poisoned rats and restored energy metabolism by repairing, to some extent, the organs injured by CO. The therapy may also improve the function of the intestinal mucosal barrier.     

Gamma aminobutyric acid radioreceptor‐assay a possible biomarker for human exposure to certain agrochemicals

Abstract

Cyclodiene insecticides, hexachlorocyclohexanes, pyrethroids, bicyclophosphates, the bicycloorthocarboxylate insecticides and some of their metabolites and environmental degradation products are central nervous system toxicants with high specific binding affinity to the chloride channel of the γ‐ aminobutyric acid (GABA)_A receptor‐ionophore sites. [³⁵S] tertiary‐butylbicyclophosphorothionate (TBPS) with specific activity higher than 60 Ci/mmole has a high binding affinity to the same sites and is now commercially available and can be used to label the GABA_A receptor for the development of a radioreceptor assay technique. The GABA receptor was prepared by ultra centnfugation and dialysis of brain homogenates of either cow, goat, rat or catfish. The receptor was then labeled with [³⁵S] TBPS and the assay was conducted by measuring the displacement of radioactivity following incubation with samples containing the analytes. A radioreceptor assay protocol was developed to measure the amount of the α‐endosulfan in blood samples. The assay was extremely sensitive, and can detect 0.2 nM of endosulfan at a level equivalent to 0.08 ppb or 8x10^‐11 gm of endosulfan in each ml of the blood samples.     

Hematological and histopathological changes in silver catfish Rhamdia quelen (Siluriformes) exposed to clomazone herbicide in the Madre River,Santa Catarina State,Southern Brazil

This study evaluated the influence of the clomazone herbicide (2-[(2-chlorophenyl)methyl]-4,4-dimethyl-3-isoxazolidinone) contamination on the hematological parameters and histological changes in gills and liver of silver catfish (Rhamdia quelen) from Madre River, Santa Catarina State, Southern Brazil. Fish were collected between March 2010 and January 2012 at two different sites of the Madre River, one site receiving residual water (contaminated site) from rice culture (n = 49) and another that do not receive residual water (reference site) (n = 48). The herbicide clomazone analysis detected 3.40 ± 1.70 μg/L in the contaminated site and 1.1 ± 0.33 μg/L in the reference site. Fish from contaminated site showed increased (P < 0.05) number of monocytes suggesting the possible defense response as a result of chronic exposure to clomazone. On the other hand, no difference was found in the hematocrit percentage, red blood cell count, total thrombocyte number, white blood cell count, lymphocytes, and neutrophils number. Fish from both sites showed histopathological changes in gills and liver, possibly caused by chronic exposure to contamination. The influence of herbicide sub doses on fish health is also discussed.     

野生与养殖长吻血液及不同器官同工酶的比较

采用聚丙烯酰胺凝胶电泳（ＰＡＧＥ－Ｅｌｅｃｔｒｏｐｈｏｒｓｉｓ）,对野生及养殖长吻Ｕａｉ心脏、肾脏、肌肉、肝脏四个器官及血液的ＬＤＨ（ＥＣ．１．１．１．２７）、ＰＯＤ（ＥＣ．１．１．１．１）、ＥＳＴ（ＥＣ．３．１．１．１）、ＭＤＨ（ＥＣ．１．１．１．３７）同工酶所获电泳图谱进行对比分析,发现以上各酶在不同组织器官中均表现出组织特异性;野生Ｕａｉ和养殖Ｕａｉ四种同工酶也存在差异;ＬＤＨ同工酶电泳带分     

Associations between maternal phthalate exposure and cord sex hormones in human infants

It has been speculated that maternal phthalate exposure may affect reproductive development in human newborns. However, the mechanism awaits further investigation. The aim is to evaluate the association between maternal phthalate exposure and cord sex steroid hormones in pregnant women and their newborns from the general population. A total of 155 maternal and infant pair were recruited and analyzed. Levels of urinary phthalate metabolites and sex steroid hormones were determined using liquid chromatography/electrospray tandem mass spectrometry (LC-ESI-MS/MS) and radioimmunoassay (RIA), respectively. No significant correlation was found between each steroid hormones and phthalate metabolites for male newborns, except MMP was marginally significantly correlated with E₂. After adjusting for maternal age, estradiol (E₂) levels in cord serum from male newborns were not correlated with maternal urinary phthalate metabolites. In female newborns, the maternal urinary levels of mono-(2-ethylhexyl) phthalate (MEHP) and mono-(2-ethyl-5-hydroxyhexyl) phthalate (5OH-MEHP) were negatively correlated with the free testosterone (fT) and fT/E₂ levels in cord serum with Pearson correlation coefficients ranging between −0.24 and −0.29 (p < 0.05). Additionally, after gestational age was adjusted, the maternal urinary level of DEHP was negatively correlated with the free testosterone (fT) and fT/E₂ levels in cord serum. We suggest that maternal exposure to phthalates may affect sex steroid hormones status in fetal and newborn stage.     

Brominated flame retardants and perfluorinated chemicals, two groups of persistent contaminants in Belgian human blood and milk

We assessed the exposure of the Flemish population to brominated flame retardants (BFRs) and perfluorinated compounds (PFCs) by analysis of pooled cord blood, adolescent and adult serum, and human milk. Levels of polybrominated diphenyl ethers (PBDEs) in blood (range 1.6-6.5 ng/g lipid weight, lw) and milk (range 2.0-6.4 ng/g lw) agreed with European data. Hexabromocyclododecane ranged between <2.1-5.7 ng/g lw in milk. Perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) dominated in blood and ranged between 1 and 171 ng/mL and <0.9-9.5 ng/mL, respectively. Total PFC levels in milk ranged between <0.5-29 ng/mL. A significant increase in PBDE concentrations was detected from newborns (median 2.1) to the adolescents and adults (medians 3.8 and 4.6 ng/g lw, respectively). An identical trend was observed for PFOS, but not for PFOA. We estimated that newborn exposure to BFRs and PFCs occurs predominantly post-natally, whereas placental transfer has a minor impact on the body burden.     

Oral administration of potassium bromate, a major water disinfection by-product, induces oxidative stress and impairs the antioxidant power of rat blood

Potassium bromate (KBrO₃) is a widely used food additive, a water disinfection by-product and a known nephrotoxic agent. The effect of KBrO₃ on rat blood, especially on the anti-oxidant defense system, was studied in this work. Animals were given a single oral dose of KBrO₃ (100 mg/kg body weight) and sacrificed 12, 24, 48, 96 and 168 h after this treatment. Blood was collected from the animals and separated into plasma and erythrocytes. KBrO₃ administration resulted in increased lipid peroxidation, protein oxidation, hydrogen peroxide levels and decreased the reduced glutathione content indicating the induction of oxidative stress in blood. Methemoglobin levels and methemoglobin reductase activity were significantly increased while the total anti-oxidant power was greatly reduced upon KBrO₃ treatment. Nitric oxide levels were enhanced while vitamin C concentration decreased in KBrO₃ treated animals. The activities of major anti-oxidant enzymes were also altered upon KBrO₃ treatment. The maximum changes in all these parameters were 48 h after the administration of KBrO₃ and then recovery took place. These results show for the first time that KBrO₃ induces oxidative stress in blood and impairs the anti-oxidant defense system. Thus impairment in the anti-oxidant power and alterations in the activities of major anti-oxidant enzymes may play an important role in mediating the toxic effects of KBrO₃ in the rat blood. The study of such biochemical events in blood will help elucidate the molecular mechanism of action of KBrO₃ and also for devising methods to overcome its toxic effects.     

Polybrominated diphenyl ethers and polychlorinated biphenyls in cord blood from women in Poland

The purpose of this study was to assess human exposure in the prenatal period to selected PBDEs (BDE-47, BDE-99, BDE-153) and PCBs (CB-77, CB-101, CB-118, CB-126, CB-138, CB-153, CB-170, CB-180) basing on the analysis of these compounds in cord blood. The experimental material consisted of 89 cord blood samples taken from women resident in Warsaw and its vicinity. In over 90% of all tested samples the presence of congeners CB-153, CB-138, CB-180 and BDE-47 was identified. The least frequently found were CB-126 and BDE-153, which were present at relatively low concentration levels. Among all analysed PCBs, the highest average concentrations were found in the case of congeners CB-138 (11.8 ng/g of fat) and CB-153 (43.4 ng/g of fat), whereas the lowest was in the case of CB-170 (0.4 ng/g of fat) and CB-126 (0.1 ng/g of fat). In the case of PBDEs the greatest share in the total concentration was that of the congeners BDE-47 and BDE-99, whereas the smallest share was that of the higher brominated congener BDE-153. These results suggest that human exposure to the examined compounds begins already in the period of intrauterine life. The comparison of our own results with the findings of other authors indicates that the PCBs and PBDEs levels in cord blood of women living in Poland do not differ from the respective concentrations in cord blood of other female inhabitants of Europe.     

Linking empirical estimates of body burden of environmental chemicals and wellness using NHANES data

Biomonitoring of industrial chemicals in human tissues and fluids has shown that all people carry a “body burden” of synthetic chemicals. Although measurement of an environmental chemical in a person's tissues/fluids is an indication of exposure, it does not necessarily mean the exposure concentration is sufficient to cause an adverse effect. Since humans are exposed to multiple chemicals, there may be a combination effect (e.g., additive, synergistic) associated with low-level exposures to multiple classes of contaminants, which may impact a variety of organ systems. The objective of this research is to link measures of body burden of environmental chemicals and a “holistic” measure of wellness. The approach is demonstrated using biomonitoring data from the National Health and Nutrition Examination Surveys (NHANES). Forty-two chemicals were selected for analysis based on their detection levels. Six biological pathway-specific indices were evaluated using groups of chemicals associated with each pathway. Five of the six pathways were negatively associated with wellness. Three non-zero interaction terms were detected which may provide empirical evidence of crosstalk across pathways. The approach identified five of the 42 chemicals from a variety of classes (metals, pesticides, furans, polycyclic aromatic hydrocarbons) as accounting for 71% of the weight linking body burden to wellness. Significant interactions were detected indicating the effect of smoking is exacerbated by body burden of environmental chemicals. Use of a holistic index on both sides of the exposure-health equation is a novel and promising empirical “systems biology” approach to risk evaluation of complex environmental exposures.