Study Set Content:
Certain toxicants are specific or neurons, resulting in their injury or death. Neuron loss is irreversible and includes degeneration of all of its cytoplasmic extensions, dendrites and axons, and the myelin unsheathing the axon • The initial injury to neurons is followed by apoptosis or necrosis, leading to permanent loss of the neuron.
o Doxorubicin o Methyl Mercury o Trimethyltin
are those in which the primary site of toxicity is the axon itself. • The toxicant results in a “chemical transection” of the axon at some point along its length, and the axon distal to the transection degenerate
AXONOPATHIES
• Certain toxicants are specific or neurons, resulting in their injury or death. Neuron loss is irreversible and includes degeneration of all of its cytoplasmic extensions, dendrites and axons, and the myelin unsheathing the axon • The initial injury to neurons is followed by apoptosis or necrosis, leading to permanent loss of the neuron. o Doxorubicin o Methyl Mercury o Trimethyltin
NEURONOPATHIES
can regenerate, whereas central axons cannot. ✓ In the PNS, () and () support axonal regeneration.
Peripheral axons, glial cells macrophages
In the CNS, release of inhibitory actors from damage myelin an astrocyte scarring actually interferes with regeneration. The clinical relevance of the disparity between the CNS an PNS is that partial to complete recovery can occur after axonal degeneration in the (), whereas the same event is () in the CNS.
PNS, irreversible
Axonopathies can be considered to result from a chemical transection of the axon. The number of axonal toxicants is large an increasing in number. As the axons regenerate, sensations and motor strength are first impaired in the most distal extent of the axonal processes (e.g., the hands and feet), resulting in a () neuropathy. With time an continue injury, the elicit progresses to involve more ()areas of the body and the long axons of the spinal cord.
“glove-an -stocking”, proximal
Humans develop a progressive sensorimotor hexane- containing glues. An identical axonopathy can be produce by methyl-n-butyl
Gamma-diketones (n-hexane)
AXONOPATHIES
Gamma-diketones (n-hexane) –
o Ketone (2-hexanone). o Carbon disulfide o IDPN (β,β′-Iminodipropionitrile) o Acrylamide o Organophosphorus compounds o Pyridinethione o Microtubule-associated Neurotoxicity
provides electrical insulation of neuronal processes, and its absence leads to a slowing of conduction and aberrant of impulses between adjacent processes
Myelin
may be caused by alterations in the transcript levels of myelin basic protein mRNA, and early in its evolution is reversible.
Intramyelinic edema
may result from progressive intramyelinic edema or from direct toxicity to the myelinating cell. It is a selective loss of myelin. o Hexachlorophene o Tellurium o Lead
Demyelination
perform and regulate a wide range of physiologic functions in the CNS. The astrocyte appears to be a primary means of defense in the CNS following exposure to neurotoxicants.
Astrocytes
Astrocytes
Ammonia o Nitrochemicals o Methionine o Sulfoximine o Fluoroacetate and Fluorocitrate
NEUROTRANSMISSION-ASSOCIATED NEUROTOXICITY
o Nicotine o Cocaine and Amphetamines o Excitatory Amino Acids
is the ultimate response of the heart to toxic exposure, which can be measured by both morphologic and functional degenerative phenotypes.
Myocardial degeneration
If acute cardiac toxicity does not affect the capacity of myocardial regeneration, the degenerative phenotype is reversible can result in cardiac arrhythmia, hypertrophy, and heart failure. o Myocardial cell death o Fibrosis (scar tissue formation), and o Contractile dysfunction
Degenerative Responses
– recent discovery of cardiac progenitor cells has challenged the view that all myocardial degeneration is permanent. These cells possess the fundamental properties of stem cells and can make myocytes and vascular structures.
Myocardial Regeneration
s an important mode o myocardial cell loss that has been demonstrated in heart failure, and myocardial infarction patients.
Apoptosis
is also important in patients with myocardial infarction and the cardiomyopathy induced by environmental toxicants and pollutants
Necrosis
An important topic of apoptotic research.
MITOCHONDRIAL CONTROL OF CELL DEATH
