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Modulation of Apoptosis by the Dithiolethione ACDT as a Neuroprotective Mechanism Against Manganese‐Induced Toxicity

Manganese (Mn) is an essential trace metal involved in metabolic processes in both animals and plants. Overexposure to this metal can cause oxidative stress leading to a neurological disorder known as manganism. Excessive accumulation of Mn is believed to cause apoptosis in cells. Apoptosis is a tightly regulated process in which cell death is induced by the activation of specific signaling pathways through numerous regulatory proteins such as Bax and Bcl‐2. Dithiolethiones are a class of sulfur‐containing heterocyclic molecules. Among them, ACDT (5‐amino‐3‐thioxo‐3H‐(1,2) dithiole‐4‐carboxylic acid ethyl ester) has been shown to induce cellular production of the natural antioxidant glutathione. It has been proven that ACDT provides neuroprotection against Mn toxicity by activating the Nrf2‐Keap1 pathway. In this study, we hypothesized that ACDT also causes upregulation of anti‐apoptotic protein Bcl‐2 and downregulation of pro‐apoptotic protein Bax as an additional mechanism of neuroprotection.