Mitochondria-associated endoplasmic reticulum membrane as a mediator of vanadium-induced endoplasmic reticulum quality control in duck brains

Vanadium (V) plays a crucial role in normal cells, but excess V causes multi-organ toxicity, including neurotoxicity. Mitochondria-associated endoplasmic reticulum membrane (MAM) is a dynamic structure between endoplasmic reticulum (ER) and mitochondria that mediates ER quality control (ERQC). To explore the effects of excess V on MAM and ERQC in the brain, 72 ducks were randomly divided into two groups: the control group (basal diet) and the V group (30 mg V/kg basal diet). On days 22 and 44, brain tissues were collected for histomorphological observation and determination of trace element contents. In addition, the mRNA and protein levels of MAM and ERQC-related factors in the brain were analyzed. Results show that excessive V causes the imbalance of trace elements, the integrity disruption of MAM, rupture of ER and autophagosomes formation. Moreover, it inhibits IP3R and VDAC1 co-localization, down-regulates the expression levels of MAM-related factors, but up-regulates the expression levels of ERQC and autophagy related factors. Together, results indicate that V exposure causes disruption of MAM and activates ERQC, which is further causing autophagy.