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doi: 10.4103/0253-7613.132160 171 JuSGeYLiPTianXWangHZhengXet al

10.1016/j.ajog.2010.01.035 58 HuC.JiaW

Combining the analysis of GSH, GSSG, and conjugates would be beneficial in pinpointing the role of contaminants within the plethora of causes that could lead to the toxic effects of reactive oxygen species

However, deletion of MLKL or inhibition of RIPK1 in macrophages does not completely rescue Mtb-infected cells from death, 84,101 suggesting that, although the deficiency of MLKL or RIPK1 can abrogate the canonical necroptosis pathway, upstream TNF/TNFR1-mediated signaling may stimulate the induction of other cell death pathways during Mtb infection