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In humans the most common initial effects of unintentional exposure are nausea, vomiting, abdominal pain, and diarrhea, though delayed seizures have been reported. [3] No antidote for bromethalin is known; care is symptomatic and supportive.
The primary antidote to brodifacoum poisoning is immediate administration of vitamin K 1 (dosage for humans: initially slow intravenous injections of 10–25 mg repeated at 3–6 hours until normalisation of the prothrombin time; then 10 mg orally four times daily as a "maintenance dose"). It is an extremely effective antidote, provided the ...
The chemical needs to be "photoactive," which means that when it absorbs light, the absorbed energy produces molecular changes that cause toxicity. Many synthetic compounds, including drug substances like tetracyclines or fluoroquinolones, are known to cause these effects.
Secondary poisoning, or relay toxicity, is the poisoning that results when one organism comes into contact with or ingests another organism that has poison in its system. It typically occurs when a predator eats an animal, such as a mouse , rat , or insect , that has previously been poisoned by a commercial pesticide .
Warning label on a tube of rat poison containing bromadiolone on a dike of the Scheldt river in Steendorp, Belgium. Bromadiolone is a potent anticoagulant rodenticide.It is a second-generation 4-hydroxycoumarin derivative and vitamin K antagonist, often called a "super-warfarin" for its added potency and tendency to accumulate in the liver of the poisoned organism.
The toxicity of L. camara to humans is undetermined, with several studies suggesting that ingesting unripe berries can be toxic to humans. [149] Other studies have found evidence which suggests that ingestion of L. camara fruit poses no risk to humans and are in fact edible when ripe. [150] Ligustrum spp. privet Oleaceae: Berries and leaves are ...
Penitrem A impairs GABAergic amino acid neurotransmission and antagonizes high-conductance Ca 2+-activated potassium channels in both humans and animals. [4] Impairment of the GABAergic amino acid neurotransmission comes with the spontaneous release of the excitatory amino acids glutamate and aspartate as well as the inhibitory neurotransmitter γ-aminobutyric acid (GABA). [4]
A study performed in 2015 with vervet monkeys (Chlorocebus sabaeus) in St. Kitts, which are homozygous for the apoE4 gene (a condition which in humans is a risk factor for Alzheimer's disease), found that vervets that were administered BMAA orally developed hallmark histopathology features of Alzheimer's disease, including amyloid beta plaques and neurofibrillary tangle accumulation.