Abstract
.We used phase microscopy and Raman spectroscopic measurements to assess the response of in vitro rat C6 glial cells following methamphetamine treatment in real time. Digital holographic microscopy (DHM) and three-dimensional (3-D) tomographic nanoscopy allow measurements of live cell cultures, which yield information about cell volume changes. Tomographic phase imaging provides 3-D information about the refractive index distribution associated with the morphology of biological samples. DHM provides similar information, but for a larger population of cells. Morphological changes in cells are associated with alterations in cell cycle and initiation of cell death mechanisms. Raman spectroscopy measurements provide information about chemical changes within the cells. Our Raman data indicate that the chemical changes in proteins preceded morphological changes, which were seen with DHM. Our study also emphasizes that tomographic phase imaging, DHM, and Raman spectroscopy are imaging tools that can be utilized for noninvasive simultaneous monitoring of morphological and chemical changes in cells during apoptosis and can also be used to monitor other dynamic cell processes.
Highlights
Methamphetamine hydrochloride (METH) is the second most widely abused illicit drug in the world
We evaluated the apoptotic effects of Doxorubicin hydrochloride (DOX), which served as a control
When cells were treated with DOX, a significant decrease in cell volume was observed within 30 min [Fig. 2(b)]
Summary
Methamphetamine hydrochloride (METH) is the second most widely abused illicit drug in the world. METH increases the release of dopamine, which induces neurotoxic responses in the human brain These neurotoxic responses can lead to neural damage and cellular apoptosis.[1,2] METH abuse results in neurotoxic damage to dopaminergic nerve terminals and leads to cellular degeneration and cell death.[3,4] Since METH is a cationic lipophilic molecule, it can diffuse through the cellular membrane to the mitochondria, resulting in the perturbation of normal mitochondrial function and the induction of mitochondrial toxicity.[4,5] This creates a buildup of positively charged molecules within the mitochondria, interfering with the electrochemical gradient established by the electron transport chain. The underlying mechanisms by which METH infiltrates the neural pathways remain enigmatic
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