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Estrogen is primarily an endocrine hormone produced by the ovaries and, to a lesser degree, glands of the adrenal cortex's zona reticularis layer. However, it can be synthesized from other tissues and can possess both autocrine and paracrine activities of the target tissue or organ. Its activities, only possible through ligand(estrogen)-receptor interaction, range from reproduction health to skeletal development. These activities can, however, be modulated by using an antagonist. An antagonist is anything that binds to the receptors to prevent the action of a particular hormone, neurotransmitter, or enzyme.The antagonist can specifically bind to the pituitary GnRH receptor, thus blocking the effect of GnRH on the pituitary and reducing the secretion of pituitary GN.Notwithstanding its numerous physiological activities, estrogen is also implicated in some cancers' pathophysiology, specifically estrogen (E2)-induced growth factor-related breast cancers. Androgen receptor, a member of the nuclear receptor superfamily, is encoded by a full-length 90 kb gene from the long arm of X chromosome 11.2–12, which contains 7 introns and 7 exons. There are two isomers of messenger RNA encoding 920 and 388 amino acid residues, respectively.This is because estrogen acts as a mediator for mitogen-activated protein kinase (MAPK/ERk) activation, facilitating cell proliferation, which can progress autonomously. This research investigates the effects of boletus poisoning on estrogen receptors and neurotransmitters in rats based on the ERk 1/2 pathway. A prospective study was conducted for which two sets of experimental studies were performed using albino rats. The first experiment was to determine the toxic dose. This is the dosage for which the saturation point will be reached and the existing estrogen on the receptors displaced. The second set of the experiment was to determine the pathophysiology of this poisoning on the albino rats. A 200 mg/100 kg b.wt oral administration of boletus spp juice and 250 mg/100 kg b.wt of alcohol extracts were administered using an oral gavage to the test specimens. The toxic effects were then recorded for the next 24 h of administration. The results indicated low levels of breast cancer markers in test specimens than those of control specimens. This is because the BoletusBoletus acted as an antagonist blocking the action of E2 on estrogen receptors (ERs). [ABSTRACT FROM AUTHOR]

Purple coneflower (Echinacea purpurea (L.) Moench) is a plant in the family Asteraceae, mainly grown in North America. Echinacea purpurea has been used in conventional medicine. The plant has immuno-stimulating and antibacterial properties, but neither mold contamination nor a mycotoxin presence have been evaluated. Our goal is to determine the degree to which molds and mycotoxins contaminate dietary supplements based on purple coneflower distributed on the Polish market. We analyzed 21 samples divided into four groups: sachets (n = 5), dry raw material (n = 3), capsules (n = 9), and tablets (n = 4). The mycological analysis of dietary supplements shows that the average number of molds is 1012 cfu/g, and the most common molds are Aspergillus spp., Phoma spp. and Eurotium spp. The mycotoxins most common in the samples are ZEN (18/21), DON (5/21) and T-2 toxin (3/21). [ABSTRACT FROM AUTHOR]

Citrinin (CIT) is a mycotoxin produced by different species of Aspergillus, Penicillium, and Monascus. CIT can contaminate a wide range of foods and feeds at any time during the pre-harvest, harvest, and post-harvest stages. CIT can be usually found in beans, fruits, fruit and vegetable juices, herbs and spices, and dairy products, as well as red mold rice. CIT exerts nephrotoxic and genotoxic effects in both humans and animals, thereby raising concerns regarding the consumption of CIT-contaminated food and feed. Hence, to minimize the risk of CIT contamination in food and feed, understanding the incidence of CIT occurrence, its sources, and biosynthetic pathways could assist in the effective implementation of detection and mitigation measures. Therefore, this review aims to shed light on sources of CIT, its prevalence in food and feed, biosynthetic pathways, and genes involved, with a major focus on detection and management strategies to ensure the safety and security of food and feed. [ABSTRACT FROM AUTHOR]