HIV-1 Tat Impairment of Mitochondrial Respiration via Complexes I and II Can Be Ameliorated by Allopregnanolone in Opioid-Exposed or Opioid-Naïve Cells and Mice DOI Creative Commons
Fakhri Mahdi,

Zia Shariat‐Madar,

Jason J. Paris

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(4), P. 420 - 420

Published: March 31, 2025

HIV-associated neurocognitive disorders are prevalent despite antiretroviral intervention. Some HIV virotoxins, such as the trans-activator of transcription (Tat), not targeted by antiretrovirals, and their neurotoxic actions may be exacerbated opioids. Both Tat morphine disrupt mitochondrial function, which promote neurotoxicity, but mechanisms poorly understood. Herein, we assess capacity to alter fundamental ability mitochondria generate transfer energy along electron transport chain (ETC). We find that exposure inhibits respiration driven ETC complexes I or II in a concentration-dependent manner. Findings were consistent across models permeabilized neuroblastoma cells, murine-derived mitoplasts, derived from mice exposed vivo. In cell culture models, promoted Ca2+ influx generation cytosolic reactive oxygen species (ROS). Acute exerted no effect on respiration, modestly offset Tat-mediated effects complex some for ROS. Morphine did exert any protective when acutely administered The mitoprotective steroid, allopregnanolone (AlloP), increased cells (complex I) mitoplasts II) attenuated impairment AlloP further intracellular ROS production. Taken together, these results suggest compromises function through respiratory physiological effects.

Language: Английский

The Essential Role of Mitochondrial Dynamics in Viral Infections DOI Open Access
Xujie Duan, Rui Liu, Wenjun Lan

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(5), P. 1955 - 1955

Published: Feb. 24, 2025

Mitochondria are dynamic organelles that play crucial roles in energy production, metabolic balance, calcium homeostasis, apoptosis, and innate immunity, key determinants of cell fate. They also targets for viral invasion the body. Many proteins target mitochondria, controlling mitochondrial morphology, metabolism, immune response, thereby achieving evasion, promoting their proliferation, accelerating infection process. Mitochondrial quality control is to maintaining normal physiological functions homeostasis. Dysregulation dynamics closely related development many diseases. New constantly being discovered. Viruses change by targeting mitochondria achieve a persistent state infection. Currently, understanding during limited. Research on impact provides foundation investigating pathogenesis infections, disease process, identifying potential therapeutic targets. This review focuses connection between priority areas research virus-mediated insight into regulation viruses explores means mitochondrial-mediated treatment

Language: Английский

Citations

0
Mitochondria-dependent innate immunity: A potential therapeutic target in Flavivirus infection DOI

Saurabh Losarwar,

Bhaskaranand Pancholi, R. Ramesh Babu

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 154, P. 114551 - 114551

Published: March 31, 2025

Language: Английский

Citations

0
HIV-1 Tat Impairment of Mitochondrial Respiration via Complexes I and II Can Be Ameliorated by Allopregnanolone in Opioid-Exposed or Opioid-Naïve Cells and Mice DOI Creative Commons
Fakhri Mahdi,

Zia Shariat‐Madar,

Jason J. Paris

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(4), P. 420 - 420

Published: March 31, 2025

HIV-associated neurocognitive disorders are prevalent despite antiretroviral intervention. Some HIV virotoxins, such as the trans-activator of transcription (Tat), not targeted by antiretrovirals, and their neurotoxic actions may be exacerbated opioids. Both Tat morphine disrupt mitochondrial function, which promote neurotoxicity, but mechanisms poorly understood. Herein, we assess capacity to alter fundamental ability mitochondria generate transfer energy along electron transport chain (ETC). We find that exposure inhibits respiration driven ETC complexes I or II in a concentration-dependent manner. Findings were consistent across models permeabilized neuroblastoma cells, murine-derived mitoplasts, derived from mice exposed vivo. In cell culture models, promoted Ca2+ influx generation cytosolic reactive oxygen species (ROS). Acute exerted no effect on respiration, modestly offset Tat-mediated effects complex some for ROS. Morphine did exert any protective when acutely administered The mitoprotective steroid, allopregnanolone (AlloP), increased cells (complex I) mitoplasts II) attenuated impairment AlloP further intracellular ROS production. Taken together, these results suggest compromises function through respiratory physiological effects.

Language: Английский

Citations

0