Exploring research gaps and trends in the management of acute phosphide poisoning: a systematic review.

Metal phosphides are highly toxic pesticides that result in high morbidities and mortalities worldwide. This systematic review included 350 studies that fulfilled the eligibility criteria. There were significant rising trends of studies on acute aluminum phosphide (AlP) and zinc phosphide (Zn3P2) poisoning (p-values = <.001), pointing to an increased number of phosphide-intoxicated patients. Acute AlP poisoning studies represented 81%, 89.3%, and 97.7% of all descriptive, analytical, and experimental interventional studies included in this review, respectively. High AlP poisoning mortality explains great research interest in AlP poisoning. Thus, after 2016, nearly half (49.7%) of studies on acute AlP poisoning were issued. Also, 78.82% of experimental interventional studies on AlP poisoning were published after 2016. The trends of in-vitro, animal, and clinical studies on AlP poisoning significantly increased with p-values equal to .021, <.001, and <.001, respectively. Seventy-nine treatment modalities for acute AlP poisoning were pooled from 124 studies; 39 management-related case reports, 12 in-vitro studies, 39 animal studies, and 34 clinical studies. All therapeutic modalities were summarized to formulate an integrated and comprehensive overview. For clinicians, therapeutic modalities significantly decreased mortality of acute AlP poisoning in clinical trials included extracorporeal membrane oxygenation (ECMO), N-acetyl cysteine (NAC), vitamin E, glucose-insulin-potassium (GIK) infusion, fresh packed RBCs infusion, and GIT decontamination using oils. However, meta-analyses are needed to provide solid evidence regarding their efficacies. To date, there is no effective antidote nor evidence-based standardized protocol for managing acute AlP poisoning. This article outlined the potential research gaps in phosphide poisoning that might promote and direct future medical research in this context.

The possible thyroid disruptive effect of di-(2-ethyl hexyl) phthalate and the potential protective role of selenium and curcumin nanoparticles: a toxicological and histological study.

Di-(2-ethylhexyl) phthalate (DEHP) is one of the ubiquitous pollutants worldwide. This study aimed to clarify the potential thyroid disrupting effect of DEHP and explore the probable ameliorative effects of selenium nanoparticles (Se-NPs) and curcumin nanoparticles (CUR-NPs). Forty-two male albino rats were divided into seven groups (n = 6): Group I (negative control); group (II) orally received DEHP (500 mg/kg BW, dissolved in corn oil); Group (III) orally received Se-NPs (.2 mg/kg BW) in combination with DEHP; Group (IV) orally received CUR-NPs (15 mg/kg BW) alongside with DEHP; Group V (corn oil); Group VI (Se-NPs) and Group VII (CUR-NPs). The duration of the experiment was 30 days. DEHP administration significantly decreased serum free T4 and significantly increased serum free T3 as compared to control group, whereas thyroid-stimulating hormone showed no significant change. DEHP disrupted redox status leading to accumulation of malondialdehyde and depletion of reduced glutathione. Histologically, the effect of DEHP on thyroid follicles was confirmed by light and electron microscopic examination and morphometric analysis. Se-NPs slightly improved thyroid parameters as well as redox status. CUR-NPS reinstated the values of all studied thyroid parameters to nearly control levels. This research provides Se-NPs and CUR-NPs as novel protective agents against DEHP-thyroid disrupting effects.

Evaluation of possible molecular toxicity induced by occupational exposure to lead and concomitant effect of smoking.

One of the most toxic heavy metals in the environment nowadays is lead (Pb). Even though exposure to lead has been reduced in some developed countries, individuals working in certain occupations are still exposed to lead at dangerous levels. Occupational exposure is of great concern and is also the main cause of lead poisoning. Although experts in various fields have been investigating the toxic effects of lead and its compounds for many years now, the association between chronic lead exposure and geno-toxicity is still an interesting point of research. The study aims to evaluate the possible DNA damage and the oxidative stress status induced by occupational exposure to lead and the role of concomitant smoking. The study was conducted on 60 subjects divided into two groups: an exposed group (40 male workers exposed to lead in their workplaces). This group was further divided into two subgroups; 20 workers were cigarette smokers and the other 20 workers were non-smokers. The other control group consists of 20 healthy males, not exposed to lead and matched by age to the exposed group (10 were smokers and the rest were non-smokers). Venous blood samples were collected from each participant for the determination of the following: blood lead level (BLL), plasma malondialdehyde (MDA) levels, and DNA damage using agarose gel electrophoresis. The exposed workers had significantly higher levels of lead and MDA, as well as a high frequency of DNA fragmentation. Smoking workers showed a greater frequency of DNA fragmentation than non-smokers. A significant relation was revealed between the BLL, as well as the MDA level, and the degree of DNA fragmentation among the lead-exposed workers. The study has shown additional evidence proving the association between Pb exposure and oxidative stress. The results further reinforced the role of cigarette smoking in augmenting such oxidative damage in the Pb-exposed population. However, further studies are recommended to evaluate the effect of cigarette smoking on Pb-exposed workers.