Excessive Cu deteriorates arsenite-induced apoptosis in chicken brain and resulting in immunosuppression, not in homeostasis.

08:00 EDT 4th September 2019 | BioPortfolio

Summary of "Excessive Cu deteriorates arsenite-induced apoptosis in chicken brain and resulting in immunosuppression, not in homeostasis."

Trace elements such as copper (Cu) and arsenic (As) are two of the major contaminants and well-known inducers of cognitive deficits and neurobehavioral changes. This study evaluated the immunotoxicity of their individual or combined exposure on different brain regions in chickens. Consequently, nuclear damage and organelle lesions, especially mitochondria were observed under Cu or/and As stress, in which positive regulation of key proteins, dynamin-related protein 1 (Drp1), Cytochrome C (Cyt c), BCL2-associated X (Bax), Caspases 3 and P53 was detected by qRCR and Western blot analyses, indicating disturbed mitochondrial dynamic equilibrium and apoptosis execution. In addition, qRCR analysis confirmed the involvement of cytokines secreted by different populations of helper T cells, indicative of cellular immunity. Gene expression studies showed marked up regulation of Th1/Th17 cytokines along with heat shock protein (HSP) 70, a synergism was noted in co-administration group. Interesting, lower apoptosis index was noted in brainstem compared to cerebrum and cerebellum. An intense immunosuppression and heat shock response against Cu or/and As was also seen in cerebrum and cerebellum but not in brainstem. In conclusion, our study suggests a synergistic neurotoxicity in chickens under Cu and As exposure. These findings provide a basic understanding of mitochondrial abnormality-initiated neuropathology in response to environmental pollutant mixtures, suggesting an adaptive response to the frangibility of the central nerve system.


Journal Details

This article was published in the following journal.

Name: Chemosphere
ISSN: 1879-1298
Pages: 124758


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Medical and Biotech [MESH] Definitions

Efflux pumps that use the energy of ATP hydrolysis to pump arsenite across a membrane. They are primarily found in prokaryotic organisms, where they play a role in protection against excess intracellular levels of arsenite ions.

Oxidoreductases that specifically reduce arsenate ion to arsenite ion. Reduction of arsenate is a critical step for its biotransformation into a form that can be transported by ARSENITE TRANSPORTING ATPASES or complexed by specific sulfhydryl-containing proteins for the purpose of detoxification (METABOLIC DETOXIFICATION, DRUG). Arsenate reductases require reducing equivalents such as GLUTAREDOXIN or AZURIN.

A c-jun amino-terminal kinase that is found predominantly within NEURONS of the BRAIN, suggesting a role in stress-induced neuronal APOPTOSIS. Several isoforms of the protein with molecular sizes of 47 kDa and 52 kDa exist due to multiple ALTERNATIVE SPLICING.

Bleeding within the brain as a result of penetrating and nonpenetrating CRANIOCEREBRAL TRAUMA. Traumatically induced hemorrhages may occur in any area of the brain, including the CEREBRUM; BRAIN STEM (see BRAIN STEM HEMORRHAGE, TRAUMATIC); and CEREBELLUM.

A member of the TNF receptor family that was initially identified as a DEXAMETHASONE-induced protein from a T-CELL line. It may play a role in regulating APOPTOSIS and modulating immune response by T-lymphocytes. Signaling by the activated receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.

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