An updated systematic review and dose-response meta-analysis on the relation between exposure to arsenic and risk of type 2 diabetes.

Arsenic is among the most critical environmental toxicants associated with many human disorders. However, its effect on type 2 diabetes mellitus (T2DM) is contradictory. This systematic review and dose-response meta-analysis aim to update information on the association between arsenic exposure and the risk of T2DM. The sample type (drinking water, urine, blood, and nails) conducted the subgroup analysis. Evaluation of the high vs. low arsenic concentrations showed a significant association between drinking water arsenic (OR: 1.58, 95% CI: 1.20-2.08) and urinary arsenic (OR: 1.37, 95% CI: 1.24-1.51) with the risk of T2DM. The linear dose-response meta-analysis showed that each 1 µg/L increase in levels of drinking water arsenic (OR: 1.01, 95% CI: 1.00-1.01) and urinary arsenic (OR: 1.01, 95% CI: 1.00-1.02) was associated with a 1% increased risk of T2DM. The non-linear dose-response analysis indicated that arsenic in urine was associated with the risk of T2DM (Pnon-linearity<0.001). However, this effect was not statistically significant for arsenic in drinking water (Pnon-linearity=0.941). Our findings suggest that blood arsenic was not significantly linked to the increased risk of T2DM in high vs. low (OR: 1.21, 95% CI: 0.85-1.71), linear (OR: 1.04, 95% CI: 0.99-1.09), and non-linear (Pnon-linearity=0.365) analysis. Also, nail arsenic was not associated with the risk of T2DM in this meta-analysis (OR: 1.33, 95% CI: 0.69-2.59). This updated dose-response meta-analysis indicated that arsenic exposure was significantly correlated with the risk of T2DM.

The electrocardiographic, hemodynamic, echocardiographic, and biochemical evaluation of treatment with edaravone on acute cardiac toxicity of aluminum phosphide.

Aluminum phosphide (AlP) poisoning can be highly fatal due to its severe toxicity to the heart. Based on the evidence, edaravone (EDA) has protective effects on various pathological conditions of the heart. This research aimed to examine the potential protective effects of EDA on AlP-induced cardiotoxicity in rats. The rats were divided into six groups, including almond oil (control), normal saline, AlP (LD50), and AlP + EDA (20, 30, and 45 mg/kg). Thirty minutes following AlP poisoning, the electrocardiographic (ECG), blood pressure (BP), and heart rate (HR) parameters were examined for 180 min. The EDA was injected 60 min following the AlP poisoning intraperitoneally. Also, 24 h after poisoning, echocardiography was carried out to evaluate the ejection fraction (EF), stroke volume (SV), and cardiac output (CO). The biochemical and molecular parameters, such as the activities of the mitochondrial complexes, reactive oxygen species (ROS), apoptosis and necrosis, and troponin I and lactate levels, were also examined after 12 and 24 h in the heart tissue. According to the results, AlP-induced ECG abnormalities, decrease in blood pressure, heart rate, SV, EF%, and CO were significantly improved with EDA at doses of 30 and 45 mg/kg. Likewise, EDA significantly improved complex I and IV activity, apoptosis and necrosis, ROS, troponin I, and lactate levels following AlP-poisoning (p < 0.05). Also, the mean survival time was increased following EDA treatment, which can be attributed to the EDA's protective effects against diverse underlying mechanisms of phosphine-induced cardiac toxicity. These findings suggest that EDA, by ameliorating heart function and modulating mitochondrial activity, might relieve AlP-induced cardiotoxicity. Nonetheless, additional investigations are required to examine any potential clinical advantages of EDA in this toxicity.

Association of maternal intake of nitrate and risk of birth defects and preterm birth: a systematic review and dose-response meta-analysis.

In this study, the high versus low analysis method was applied to evaluate the association of maternal nitrate intake and risk of heart defect, limb deficiency, cleft lip, and preterm birth. Also, linear and non-linear dose-response associations between maternal intake of nitrate and risk of heart defects were investigated. In high versus low intake, the risk of heart defects in infants is directly associated with the level of nitrate exposure, but no significant relationship was found between the cleft lip, limb deficiency, and preterm birth. The linear dose-response meta-analysis was associated with risk of heart defects (RR: 1.03; 95% CI: 1.00 to 1.05, P = 0.400, I2= 0%, P heterogeneity= 0.602, n = 3) and nonlinear dose-response meta-analysis showed that maternal intake of nitrate higher than ∼4 mg/day is positively associated with heart defects risk (P non-linearity= 0.012).

Development of effervescence-assisted switchable polarity solvent homogeneous liquid-phase microextraction for the determination of permethrin and deltamethrin in water samples prior to gas chromatography-flame ionization detection.

An effervescent tablet-assisted switchable polarity solvent-based homogeneous liquid-phase microextraction combined with gas chromatography with flame ionization detection has been conducted for the separation, preconcentration, and detection of permethrin and deltamethrin in the river water specimens. Triethylamine (TEA) was utilized as the switchable polarity solvent in this method. The switching process was carried out by the dissolution of an effervescent tablet including an effervescency agent (sodium carbonate) and a proton donor agent (citric acid). Changing the pH of the specimen solution enhanced the conversion of TEA into protonated triethylamine carbonate through the tablet that generated carbon dioxide bubbles in situ. Finally, the addition of sodium hydroxide changed the ionization state of TEA and separated the two phases. Influential factors in the extraction were investigated. According to optimal situations, the limit of detection and the limit of quantification were 0.16 and 0.5 µg L-1 for permethrin and 0.03 and 0.1 µg L-1 for deltamethrin, respectively. The preconcentration factor was 194 in river water samples and inter- and intra-day precision (relative standard deviation %; n = 5) was <5%. The extraction recovery was obtained in the range of 93.0%-97% for permethrin and deltamethrin in water samples.

Method development for determination of imatinib and its major metabolite, N-desmethyl imatinib, in biological and environmental samples by SA-SHS-LPME and HPLC.

A salting-out-assisted switchable hydrophilicity solvent-based liquid phase microextraction (SA-SHS-LPME) was developed for the separation and determination of trace amounts of imatinib and N-desmethyl imatinib in biological and environmental samples by HPLC-UV. Triethylamine as a hydrophobic compound and protonated triethylamine carbonate as a hydrophilic one were switched by the addition or elimination of CO2 . The use of NaOH resulted in the elimination of CO2 from the sample solution, which led to the conversion of P-TEA-C into triethylamine (TEA) and as a result, the analytes was extracted and entered the TEA phase. The salting out was performed to speed up the formation of the TEA in the shape of fine droplets in the specimen solution. Furthermore, the impact of several momentous factors that influence the recovery of the extraction was investigated. Under the optimum conditions, the limit of detection and limit of quantification were obtained in ranges of 0.03-0.05 and 0.1-0.15 µg L-1 for imatinib and 0.04-0.06 and 0.13-0.20 µg L-1 for N-desmethyl imatinib, respectively. The preconcentration factor was 250. Inter- and intraday precision (RSD, n = 5) was <5%. In the case of imatinib and N-desmethyl imatinib in biological and environmental specimens, a range of 97.0-102% was obtained as the recovery.