Journal of ethnopharmacology
August 30, 2012
Roman Paškulin, Polona Jamnik, Tjaša Danevčič et al.
19 citations
Ibogaine, a compound from the iboga plant, temporarily increases cellular energy consumption and carbon dioxide production in a dose-dependent manner, as shown in a yeast model. This energy mobilization paradoxically reduces the ATP pool while simultaneously lowering overall oxidative load. Ibogaine does not act as a direct antioxidant but instead stimulates the cell's own oxidative stress defense systems, leading to metabolic remodeling. The initial energy cost results in improved efficiency of antioxidative systems, reduced oxidative damage, and lower basal metabolic needs. This new metabolic equilibrium saves energy and makes it readily available for extra demands, suggesting benefits for health, stress resistance, and recovery from diseases including addiction.
Life (Basel, Switzerland)
December 23, 2021
Nikola Tatalović, Teodora Vidonja Uzelac, Milica Mijović et al.
8 citations
In female rats, ibogaine treatment produced lower liver glycogen breakdown than previously seen in males, along with dilation of liver blood vessels and increased thiol concentrations six hours after dosing. After 24 hours, liver catalase activity and lipid peroxidation rose while xanthine oxidase activity fell. Kidneys showed mild damage, decreased glutathione reductase, and increased catalase and xanthine oxidase activity at various time points. Ibogaine did not alter antioxidant enzymes in red blood cells. Bioavailability of ibogaine was two to three times higher in females than males. Effects were sex- and tissue-specific, and also dose- and time-dependent.
Archives of Biological Sciences
December 5, 2018
Teodora Vidonja Uzelac, Nikola Tatalović, Milica Mijović et al.
7 citations
A single oral dose of ibogaine (1 or 20 mg/kg body weight) in rats did not alter the activities of superoxide dismutases, catalase, glutathione peroxidase, glutathione reductase, or glutathione-S-transferase in the liver or erythrocytes at 6 or 24 hours after administration. However, hepatic xanthine oxidase activity increased in rats receiving 20 mg/kg, indicating faster adenosine turnover. TBARS concentration rose in the 1 mg/kg group after 24 hours, suggesting mild oxidative stress. Histological examination revealed glycogenolytic activity in hepatocytes, peaking at 24 hours in the higher-dose group. Ibogaine influenced hepatic redox homeostasis but not enough to remodel antioxidant enzyme activities within the timeframe studied.
Oxidative medicine and cellular longevity
January 1, 2018
Zorana Oreščanin-dušić, Nikola Tatalović, Teodora Vidonja-Uzelac et al.
7 citations
Ibogaine, an alkaloid from the African shrub Tabernanthe iboga, alters uterine muscle activity in a concentration-dependent way. Low concentrations stimulate spontaneous contractions, while higher doses inhibit them. Inhibitory doses reduce SOD1 activity and increase GSH-Px activity; complete inhibition raises CAT activity. These enzyme changes are due to posttranslational modifications, not altered protein levels, and point to a large rise in hydrogen peroxide. Since extracellular ATP stimulates uterine contractions and hydrogen peroxide inhibits them, ibogaine's dual effect likely stems from its known impact on cellular ATP levels and redox balance.
International journal of molecular sciences
June 13, 2024
Teodora Vidonja Uzelac, Nikola Tatalović, Milica Mijović et al.
6 citations
Ibogaine, an alkaloid used in alternative addiction treatment, caused dose-dependent heart muscle cell death (necrosis) in rats 6 and 24 hours after a single oral dose of 1 or 20 mg/kg. This cardiotoxicity was not driven by inflammation. No consistent changes in antioxidant defenses or oxidative damage markers were observed, leaving the role of oxidative stress in ibogaine-induced heart damage unclear. The findings help explain the often-fatal cardiac side effects seen in humans using ibogaine, but definitive conclusions about redox processes require further study.
Antioxidants (Basel, Switzerland)
November 9, 2021
Nikola Tatalović, Teodora Vidonja Uzelac, Zorana Oreščanin Dušić et al.
5 citations
A single dose of ibogaine (28.8 μmol/L) applied to isolated rat uterus altered contractility and antioxidant enzyme activity over four hours. In spontaneously contracting uteri, ibogaine immediately increased contraction amplitude and frequency, effects blocked by propranolol (β-adrenoceptor antagonist) and glibenclamide (KATP channel inhibitor, for frequency only). In calcium-stimulated uteri, ibogaine decreased amplitude and frequency after four hours; propranolol prevented the amplitude reduction, but glibenclamide had no effect. Ibogaine reduced superoxide dismutase 1 (SOD1) activity and increased catalase (CAT) activity after two hours in both uterus types, and in calcium-stimulated uteri also reduced SOD2 activity. After four hours, SOD1 returned to baseline while glutathione peroxidase (GSH-Px) activity rose. Pre-treatment with propranolol or glibenclamide abolished these enzyme changes, indicating ibogaine's pro-antioxidant effects are mediated by β-adrenergic receptors and KATP channels.
Archives of Biological Sciences
January 1, 2019
Teodora Vidonja Uzelac, Nikola Tatalović, Milica Mijović et al.
4 citations
A single oral dose of ibogaine (1 or 20 mg/kg body weight) in rats altered kidney antioxidant enzyme activities and caused mild morphological changes without affecting overall kidney function. The lower dose increased superoxide dismutase 1 activity and decreased glutathione reductase activity at 6 and 24 hours; the higher dose also decreased glutathione reductase activity, indicating disrupted redox balance. After 24 hours, moderate structural changes in kidney tissue were observed, but urinalyses showed no impairment of kidney function. The authors advise monitoring kidney function during and after ibogaine use in humans.
Brazilian Archives of Biology and Technology
January 1, 2021
Elvira Vukašinović, Jelena Purać, Danijela Kojić et al.
2 citations
The effects of ibogaine on antioxidant mechanisms remain incompletely understood. Using honey bee midgut as an ex vivo model system, ibogaine treatment induced up-regulation of the Sod1 gene, indicating a pro-antioxidant action.
IBRO Reports
December 1, 2019
Nikola Tatalović, Teodora Vidonja Uzelac, Zorana Oreščanin-dušić et al.
A single oral dose of ibogaine (20 mg/kg) in female Wistar rats caused transient oxidative stress in the brain and depleted glycogen stores in the liver. Six hours after treatment, lipid peroxidation (TBARS) increased significantly, while after 24 hours it returned to control levels. Protein free sulfhydryl groups increased, but nonprotein free sulfhydryl groups (indicating reduced glutathione) decreased, both more pronounced at 24 hours. Despite these signs of oxidative stress, the activities of antioxidative enzymes (SOD, CAT, GSH-Px, GR) and glutathione S-transferases remained unchanged. Liver glycogen was reduced, more at 6 hours than at 24 hours, suggesting a transient depletion of energy reserves that begins to recover within a day. These findings suggest ibogaine induces rapid, reversible changes in redox and energy homeostasis.