@article{fdi:010062612, title = {{A} feedback mechanism to control apoptosis occurs in the digestive gland of the {O}yster {C}rassostrea gigas exposed to the paralytic shellfish toxins producer {A}lexandrium catenella}, author = {{R}olland, {J}. {L}. and {M}edhioub, {W}. and {V}ergnes, {A}. and {A}bi-{K}halil, {C}. and {S}avar, {V}. and {A}badie, {E}. and {M}asseret, {E}stelle and {A}mzil, {Z}. and {L}aabir, {M}.}, editor = {}, language = {{ENG}}, abstract = {{T}o better understand the effect of {P}aralytic {S}hellfish {T}oxins ({PST}s) accumulation in the digestive gland of the {P}acific oyster, {C}rassostrea gigas, we experimentally exposed individual oysters for 48 h to a {PST}s producer, the dinoflagellate {A}lexandrium catenella. {I}n comparison to the effect of the non-toxic {A}lexandrium tamarense, on the eight apoptotic related genes tested, {B}ax and {BI}.1 were significantly upregulated in oysters exposed 48 h to {A}. catenella. {A}mong the five detoxification related genes tested, the expression of cytochrome {P}450 ({CYP}1{A}) was shown to be correlated with toxin concentration in the digestive gland of oysters exposed to the toxic dinoflagellate. {B}eside this, we observed a significant increase in {ROS} production, a decrease in caspase-3/7 activity and normal percentage of apoptotic cells in this tissue. {T}aken together, these results suggest a feedback mechanism, which may occur in the digestive gland where {BI}.1 could play a key role in preventing the induction of apoptosis by {PST}s. {M}oreover, the expression of {CYP}1{A}, {B}ax and {BI}.1 were found to be significantly correlated to the occurrence of natural toxic events, suggesting that the expression of these genes together could be used as biomarker to assess the biological responses of oysters to stress caused by {PST}s.}, keywords = {shellfish ; toxin ; biomarker ; expression ; phytoplankton ; {PACIFIQUE}}, booktitle = {}, journal = {{M}arine {D}rugs}, volume = {12}, numero = {9}, pages = {5035--5054}, ISSN = {1660-3397}, year = {2014}, DOI = {10.3390/md12095035}, URL = {https://www.documentation.ird.fr/hor/fdi:010062612}, }