No abstract

No abstract

No abstract

Aluminum phosphide (AlP) poisoning can be deadly in most cases targeting the heart. To overcome AlP toxicity, exenatide has been studied in the present study due to its pleiotropic effects on cardiac damages. In this study, the rats were exposed to LD50 of AlP (10 mg/kg) by gavage, and exenatide at doses (0.05, 0.1, and 0.2 mg/kg) injected intraperitoneally 30 min after poisoning. The cardiac parameters including heart rate (HR), blood pressure (BP), QRS, corrected QT (QTc), and ST were monitored for 180 min. Blood glucose level was measured in the study groups 30 min after exenatide injection. Evaluation of biochemical parameters including mitochondrial complexes I, II, and IV activities, adenosine diphosphate (ADP)/adenosine triphosphate (ATP) ratio, malondialdehyde (MDA), apoptosis, lactate, troponin I, and brain natriuretic peptide (BNP) was done on heart tissues after 12 and 24 h. Additionally, the tissues were analyzed for any pathological damages including necrosis, hemorrhage, or hyperemia 24 h post-treatment. Our results showed that AlP-induced HR, BP, and electrocardiographic changes were improved by exenatide at all doses. The blood glucose levels of poisoned animals reached control levels after exenatide treatment. Besides, treatment with exenatide at all doses improved complexes I and IV activity, ADP/ATP ratio, and apoptosis. Malondialdehyde, lactate, troponin I, and BNP levels were also diminished after exenatide co-treatment in poisoned animals. On the other hand, administration of exenatide doses improved the histopathology of AlP-induced tissues. Based on our findings, exenatide has a protective effect against phosphine-induced cardiotoxicity in an almost dose-dependent way. However, further investigations are needed on the potential clinical use of exenatide in this poisoning.

No abstract

Background: Various anticancer drugs are effective therapeutic agents for cancer treatment; however, they cause severe toxicity in body organs. Cardiotoxicity is one of the most critical side effects of these drugs. Based on various findings, turmeric extract has positive effects on cardiac cells. Objective: This study aims to evaluate how curcumin as the main component of turmeric may affect chemotherapy-induced cardiotoxicity. Method: Database search was performed up to April 2021 using “curcumin OR turmeric OR Curcuma longa” and “chemotherapy-induced cardiac disease,” including all their equivalents and similar terms. After screening the total articles obtained from the electronic databases, 25 relevant articles were included in this systematic review. Results: The studies demonstrate lower body weight and increased mortality rates due to doxorubicin administration. Besides, cancer therapeutic agents induced various morphological and biochemical abnormalities compared to the non-treated groups. Based on most of the obtained results, curcumin at nontoxic doses can protect the cardiac cells mainly through modulating antioxidant capacity, regulation of cell death, and anti-inflammatory effects. Nevertheless, according to a minority of findings, curcumin increases the susceptibility of the rat cardiomyoblast cell line (H9C2) to apoptosis triggered by doxorubicin. Conclusion: According to most nonclinical studies, curcumin can have the potential of cardioprotective effects against cardiotoxicity induced by chemotherapy. However, based on limited, contradictory findings demonstrating the function of curcumin in potentiating doxorubicin-induced cardiotoxicity, well-designed studies are needed to evaluate the safety and effectiveness of treatment with new formulations of this compound during cancer therapy.

BackgroundDiabetes-induced reproductive complications can lead to subfertility and infertility, raising the need to protect reproductive organs. There are limited medications used to improve reproductive health in diabetic patients. Melatonin, mainly produced by the pineal gland, may improve diabetes-associated reproductive complications through various mechanisms and may be a preferred candidate to protect the reproductive system. The present review aims to elucidate the underlying mechanisms of melatonin’s effect on the reproductive system adversely affected by diabetes mellitus (DM).MethodsA comprehensive systematic literature electronic search was done using the PRISMA guidelines. Web of Science, PubMed, Embase, and Scopus were searched for publications up to June 2022. Search terms were selected based on the study purpose and were explored in titles and abstracts. After screening, out of a total of 169 articles, 14 pertinent articles were included based on our inclusion and exclusion criteria.ResultsThe results of studies using rats and mice suggest that DM adversely affects reproductive tissues, including testes and epididymis, prostate, corpus cavernosum, and ovary leading to alterations in histological and biochemical parameters compared to the normal groups. Treatment with melatonin improves oxidative stress, blocks apoptosis induced by endoplasmic reticulum stress and caspase activation, reduces pro-inflammation cytokines, and enhances steroidogenesis.ConclusionMelatonin exerted a protective action on the impaired reproductive system in in-vivo and in-vitro models of DM. The topic has to be followed up in human pregnancy cases that will need more time to be collected and approved.

A class of organic chemicals known as polychlorinated biphenyls (PCBs) consists of chlorine, hydrogen, and carbon atoms. High boiling points, chemical stability, non-flammability, and insulating properties have enabled them to be used in various industries. Because of their high toxicity, PCBs were one of the first industrial compounds to be banned from production. These compounds have high-fat solubility with bioaccumulation and biomagnification properties in the environment, food chain, and individuals. Hence, they may have an impact not only on individual organisms but ultimately on whole ecosystems. The main sources of PCB exposure are food and environmental pollutants. In the toxicology of PCBs, oxidative stress plays the most influential function. The induction of CYP1A1 due to the high affinity of PCBs for aryl hydrocarbon receptors is considered a trigger for oxidative stress. Production of reactive oxygen species and depletion of glutathione occur due to phase Ⅰ and Ⅱ metabolism, respectively. Thus, cellular redox balance may be disrupted in the presence of PCBs and their metabolites. Chronic and long-term exposure to these compounds can often lead to life-threatening diseases, like diabetes, obesity, cardiovascular and neurological diseases, cancer, and reproductive and endocrine disorders. We present the current knowledge of the routes of PCB exposure and bioaccumulation, the outlook regarding environmental and food safety, the potential role of PCBs in various diseases, the principal mechanisms responsible for PCB toxicity, and the main detection techniques used for PCBs.