How do toxins interact with cellular receptors?
Toxins interact with cellular receptors by binding to specific sites on the receptor proteins located on the cell surface or within the cell. This interaction can induce changes in receptor conformation, activate or inhibit signaling pathways, and ultimately disrupt normal cellular functions, leading to cell damage or death.
What are the different types of toxins and their mechanisms of action?
Toxins are classified into exotoxins, endotoxins, and mycotoxins. Exotoxins, released by bacteria, disrupt cellular functions or cause cell death. Endotoxins, part of Gram-negative bacteria cell walls, trigger immune responses leading to inflammation. Mycotoxins, produced by fungi, inhibit protein synthesis and modify immune functions, often resulting in toxicity.
How do toxins affect the nervous system?
Toxins affect the nervous system by disrupting neurotransmitter release, blocking ion channels, and causing neuronal damage or cell death. They can interfere with signal transmission, leading to symptoms like paralysis, seizures, and loss of sensation. Examples include botulinum toxin blocking acetylcholine release and tetrodotoxin inhibiting sodium channels.
How do organisms detoxify or counteract toxins?
Organisms detoxify toxins through biotransformation processes, primarily occurring in the liver, which convert harmful substances into less toxic or water-soluble compounds for excretion. Enzymes like cytochrome P450 play a key role. Additionally, antioxidant systems neutralize free radicals, and protective molecules like glutathione participate in detoxification pathways.
How do toxins cause cell damage and tissue injury?
Toxins cause cell damage by disrupting cellular processes, such as protein synthesis, membrane integrity, or signal transduction. They may generate reactive oxygen species, causing oxidative stress, or inhibit enzymes, leading to cell death. Tissue injury occurs when accumulated cellular damage disrupts organ functions, often triggering inflammatory responses.