Search

This meta-analysis evaluates the association between atrazine (ATR) exposure and small for gestational age (SGA), preterm birth (PTB), and low birth weight (LBW). A comprehensive search was done on academic databases (e.g. PubMed, Scopus, Embase, and Google Scholar) to achieve all pertinent studies up to May 2023. A pooled odd ratio (OR) and corresponding 95% confidence interval (CI) were applied to evaluate this correlation. As a result, five eligible studies met the inclusion criteria and were included in our study, and the result of the present meta-analysis showed that ATR exposure increased the risk of SGA (OR = 1.11; 95% CI = 1.03–1.20 for highest versus lowest category of ATR), PTB (OR = 1.16; 95% CI = 1.03–1.30), and LBW (OR = 1.26; 95% CI = 1.10–1.44). This meta-analysis suggests that ATR in drinking water may be a risk factor for SGA, PTB, and LBW. [ABSTRACT FROM AUTHOR]

Food additives are substances that have long been applied in processed foods, either natural or synthetic. Several purposes have been fulfilled by the application of food additives, the two most notable of which are known to be preventing food spoilage and providing specific colors and flavors. Some food additives are added to food products through direct contact, whereas the rest are added indirectly e.g., through their packaging bags. In addition to the economic and commercial benefits provided by food additives, over the past two decades, studies have demonstrated a significant correlation between excessive consumption of the foods containing such additives (e.g., BHA and BHT) and several adverse health effects, e.g., the incidence of cancer and skin conditions, among others. Through different age groups, children have been found to be the population at the highest risk for such adverse effects induced by food additives. Indeed, it has been reported that food additives may give rise to attention deficit hyperactivity disorder (ADHD) among the child population. Emerging evidence has shown that emulsifiers (e.g., carboxymethyl cellulose and polysorbate), employed as food additives, might alter gut microbiota composition, leading to ulcerative colitis, affecting immune and inflammatory responses, and mental health problems. Therefore, in this review, alongside the beneficial impact of food additives, their adverse health effects as well as their acceptable daily intake have been investigated. [ABSTRACT FROM AUTHOR]

The incidence of cancer has been growing worldwide. Better survival rates following the administration of novel drugs and new combination therapies may concomitantly cause concern regarding the long‐term adverse effects of cancer therapy, for example, second primary malignancies. Moreover, overcoming tumour resistance to anticancer agents has been long considered as a critical challenge in cancer research. Some low toxic adjuvants such as herb‐derived molecules may be of interest for chemoprevention and overcoming the resistance of malignancies to cancer therapy. Apigenin is a plant‐derived molecule with attractive properties for chemoprevention, for instance, promising anti‐tumour effects, which may make it a desirable adjuvant to reduce genomic instability and the risks of second malignancies among normal tissues. Moreover, it may improve the efficiency of anticancer modalities. This paper aims to review various effects of apigenin in both normal tissues and malignancies. In addition, we explain how apigenin may have the ability to protect usual cells against the genotoxic repercussions following radiotherapy and chemotherapy. Furthermore, the inhibitory effects of apigenin on tumours will be discussed. [ABSTRACT FROM AUTHOR]

Activin A (ActA) is a cytokine from the TGF-β superfamily that mediates a vast number of physiological mechanisms, mainly through the SMAD signaling pathway. Growing evidence indicates that ActA overexpression is also correlated with poor prognosis in cancer patients and several tumor characteristics, including cancer proliferation, metastasis, immunosuppression, drug resistance, cachexia, and cancer-associated fibroblast activation. As such, ActA-targeted therapy has been viewed as a potential adjuvant therapy alongside other anti-cancer modalities that may result in more efficient anti-cancer effects, such as stronger immune responses, overcoming drug resistance, reversing cachexia, etc. However, despite its interesting concept, targeting ActA is not without certain challenges and considerations. Indeed, ActA has unexpectedly shown anti-tumor effects in some cases, which might be explained by differences in the expression levels of different ActA receptors on the cell surface, activation of non-SMAD pathways, and imbalance in ActA levels. Besides, many of the current ActA antagonists lack enough specificity and, as a result, bind to non-ActA receptors as well. Furthermore, ubiquitous expression of ActA in the body can cause serious adverse effects following systemic administration. Furthermore, to address these issues, anti-ActA monoclonal antibodies and nanoparticle drug delivery systems have recently been suggested to target ActA with better precision in the affected area. In this review, first, we provide the different implications of ActA in cancer. Then, we discuss the recent insights into targeting ActA signaling as an adjuvant therapy alongside other anti-cancer modalities, as well as the possible challenges and novel opportunities on the path of clinical translation., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Induction of cell death and inhibition of cell proliferation in cancer have been set as some of the main goals in anti-tumor therapy. Cancer cell resistance leads to less efficient cancer therapy, and consequently, to higher doses of anticancer drugs, which may eventually increase the risk of serious side effects in normal tissues. Apigenin, a nature-derived and herbal agent, which has shown anticancer properties in several types of cancer, can induce cell death directly and/or amplify the induction of cell death through other anti-tumor modalities. Although the main mechanism of apigenin in order to induce cell death is apoptosis, other cell death pathways, such as autophagic cell death, senescence, anoikis, necroptosis, and ferroptosis, have been reported to be induced by apigenin. It seems that apigenin enhances apoptosis by inducing anticancer immunity and tumor suppressor genes, like p53 and PTEN, and also by inhibiting STAT3 and NF-κB signaling pathways. Furthermore, it may induce autophagic cell death and ferroptosis by inducing endogenous ROS generation. Stimulation of ROS production and tumor suppressor genes, as well as downregulation of drug-resistance mediators, may induce other mechanisms of cell death, such as senescence, anoikis, and necroptosis. It seems that the induction of each type of cell death is highly dependent on the type of cancer. These modulatory actions of apigenin have been shown to enhance anticancer effects by other agents, such as ionizing radiation and chemotherapy drugs. This review explains how cancer cell death may be induced by apigenin at the cellular and molecular levels., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Cancer has remained to be one of the major challenges in medicine and regarded as the second leading cause of death worldwide. Different types of cancer may resist anti-cancer drugs following certain mutations such as those in tumor suppressor genes, exhaustion of the immune system, and overexpression of drug resistance mediators, which increase the required concentration of anticancer drugs so as to overcome drug resistance. Moreover, treatment with a high dose of such drugs is highly associated with severe normal tissue toxicity. Administration of low-toxic agents has long been an intriguing idea to enhance tumor suppression. Naturally occurring agents e.g., herb-derived molecules have shown a dual effect on normal and malignant cells. On the one hand, these agents may induce cell death in malignant cells, while on the other hand reduce normal cell toxicity. Nobiletin, one of the well-known polymethoxyflavones (PMFs), has reportedly shown various beneficial effects on the suppression of cancer and the protection of normal cells against different toxic agents. Our review aims to explain the main mechanisms underlying nobiletin as an inhibitor of cancer. We have reviewed the mechanisms of cancer cell death caused by nobiletin, such as stimulation of reactive oxygen species (ROS), modulation of immune evasion mechanisms, targeting tumor suppressor genes, and modulation of epigenetic modulators, among others; the inhibitory mechanisms of nobiletin affecting tumor resistance properties such as modulation of hypoxia, multidrug resistance, angiogenesis, epithelial-mesenchymal transition (EMT) have been fully investigated. Also, the inhibition of anti-apoptotic and invasive mechanisms induced by nobiletin will later be discussed. In the end, protective mechanisms of nobiletin on normal cells/tissue, clinical trial results, and future perspectives are reviewed., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)