Table 1 The summary of neurotoxic injury through multiple molecular mechanisms

Directly attacking DNA

Zhen Luo et

Aaron M Fleming et. Chryssostomos Chatgilialoglu et

Flow cytometry and immunofluorescence were applied to pTc cell lines after exogenous ROS intervention to detect cell cycle and apoptotic proteins

Spectroscopic detection of intermediates generated by ROS damage by using an ICCD camera, measurement of purine damage by stable isotope LC–MS/MS labelling of ROS

Manifestations

Sites

ROS cause ectodermal cell cycle arrest at S and G2/M phases and increase autophagy protein expression

ROS injury DNA through sites: 8-oxo-Pu, 5carboxamido-5-formamido-2iminohydantoin

Michael A Terzidis et. Jean Cadet et

Gamma-irradiation experiments were performed on the intervened pUC19 plasmid with dsDNA samples. Quantification of purine lesions by stable isotope LCMS/MS labeling

Pathway

Damage caused by ROS to DNA: tandem

damage, intra- and interstrand crosslinks, and DNA–protein crosslinks. Injury starts at lower structures (L > OC > SC)

Neuroinflammation

María Pascual et. Lídia Cantacorps, et. Silvia AlfonsoLoeches et. María Pascual et

Cynthia J M Kane, et. Jorge

Montesinos et

C57BL/6 wild-type and TLR4-KO pregnant mice were exposed daily by drinking at timed whole-gestation intervals with 10–20% ethanol solution (v/v), 5 g/kg after which TLRs were quantified in the F1 generation by electron microscopy, ELISA

C57BL/6 J mice were exposed by gavage for the entire gestation period using 30% ethanol solution (v/v) at 4 g/kg. Quantitative analysis by immunohistochemistry, quantitative PCR

Signal transduction

Inflammatory factors

TLRs on the glial cell surface are activated by ROS thereby trigger signaling cascades to stimulate the production of inflammatory factors and effects. Activated TLRs transmits inflammatory signals through transcription factors AP-1 and NF-κB

The ACKR3, CXCL12/CXCR4/CXCR7 axis of chemokines has a prominent role in FASD,

resulting in differential biological activity and signaling activation

Guo-Qing Chang et

Kinning Poon et

Kai Zhang et

Oral exposure of rats to 2 g/kg of ethanol during early to mid-pregnancy. For the F1 generation of C57BL/6 J mice 4 days after birth 5 g/kg of ethanol saline solution (20%) was given subcutaneously four times. F1 generation progenitor neurons were cultured. Analysis of chemokines by combining electron microscopy and immunofluorescence methods

CXCL12/CXCR4, CCL2/CCR2, and the corresponding mRNAs are increased upon alcohol stimulation, which is essential for the activation and recruitment of monocyte macrophages and microglia in the embryonic CNS