The role of oxidative stress in toxicities due to drugs of abuse

Pavlek, Leeann R.; Dillard, Julie; Rogers, Lynette K.

doi:10.1016/j.cotox.2020.04.003

Cited by 9 publications

(7 citation statements)

References 57 publications

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“…Opioid exposure and withdrawal in adulthood can cause both oxidative stress as well as gene expression changes in multiple brain regions (22,25,37,39). Opioids are also highly addictive drugs with high abuse potential, and as such, readily engage reward-related brain circuitry during drug exposure (48,(55)(56)(57)(58).…”

Section: Resultsmentioning

confidence: 99%

“…In addition to the many neurobiological changes in reward related processing, and cycles of negative affect that are associated with opioid use, escalation of use, and substance use disorders (13)(14)(15)(16)(17)(18), opioid exposure is also associated with high degrees of oxidative stress and oxidative damage both centrally and peripherally (19)(20)(21)(22)(23). Patients with opioid use disorders show higher levels of oxidative and inflammatory markers in blood serum (24), and are more likely to show markers of metabolic syndrome, indicative of increased risk for mortality due to heart disease or diabetes (25).…”

Section: Introductionmentioning

confidence: 99%

“…Multiple pre-clinical studies have shown metabolic disruptions and oxidative damage in brain tissue after morphine or heroin exposure (19,26). Oxidative damage in the form of increased reactive oxygen species and decreased antioxidant enzyme activity caused by drug use can lead to mitochondrial dysfunction and neurotoxicity as well as other cellular damage (22,26). Mitochondria specifically both absorb inflammatory and metabolic damage (27)(28)(29) and mediate brain function, neuroplasticity, and early life brain development (30)(31)(32)(33)(34).…”

Section: Introductionmentioning

confidence: 99%

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Mitochondria-Related Nuclear Gene Expression in the Nucleus Accumbens and Blood Mitochondrial Copy Number After Developmental Fentanyl Exposure in Adolescent Male and Female C57BL/6 Mice

et al. 2021

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The potency of the synthetic opioid fentanyl and its increased clinical availability has led to the rapid escalation of use in the general population, increased recreational exposure, and subsequently opioid-related overdoses. The wide-spread use of fentanyl has, consequently, increased the incidence of in utero exposure to the drug, but the long-term effects of this type of developmental exposure are not yet understood. Opioid use has also been linked to reduced mitochondrial copy number in blood in clinical populations, but the link between this peripheral biomarker and genetic or functional changes in reward-related brain circuitry is still unclear. Additionally, mitochondrial-related gene expression in reward-related brain regions has not been examined in the context of fentanyl exposure, despite the growing literature demonstrating drugs of abuse impact mitochondrial function, which subsequently impacts neuronal signaling. The current study uses exposure to fentanyl via dam access to fentanyl drinking water during gestation and lactation as a model for developmental drug exposure. This perinatal drug-exposure is sufficient to impact mitochondrial copy number in circulating blood leukocytes, as well as mitochondrial-related gene expression in the nucleus accumbens (NAc), a reward-related brain structure, in a sex-dependent manner in adolescent offspring. Specific NAc gene expression is correlated with both blood mitochondrial copy number and with anxiety related behaviors dependent on developmental exposure to fentanyl and sex. These data indicate that developmental fentanyl exposure impacts mitochondrial function in both the brain and body in ways that can impact neuronal signaling and may prime the brain for altered reward-related behavior in adolescence and later into adulthood.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mitochondria-Related Nuclear Gene Expression in the Nucleus Accumbens and Blood Mitochondrial Copy Number After Developmental Fentanyl Exposure in Adolescent Male and Female C57BL/6 Mice

et al. 2021

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“…These are Psychoactive drugs. Polydrug use among adolescence is a widespread activity and has enhanced in the last some years 29 . Most nandrolone decanoate abusers combine its use with cannabis.…”

Section: Nandrolone Decanoate With Cannabismentioning

confidence: 99%

An Updated Review on Some Neurotoxic Pharmacological Agents Along with their Neurotoxic Mechanisms

Bashir¹,

Aziz²,

Noor³

2021

IJFMT

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This review will provide the vital information about some pharmacological agents which are Neurotoxic. Through this update, Anti-cancer, Anti-bacterial, Analgesic, Psychoactive drug and Anabolic steroid medication are reported briefly regarding their neurotoxic mechanisms. In this review all information regarding neurotoxic drugs is collected from 2020 published work by Web of science, Scopus, PubMed and Google Scholar. It is concluded that all these drugs which the part of our study are neurotoxic. There is need to discover some method to reduce their toxicity and to avoid the chronic use of these medications.

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“…Addiction also includes a desire for the substances and, in some situations, participation in potentially fatal dangerous actions (3).Because the brain is one of the most metabolically active tissues, it is highly vulnerable to toxicity. In addition to other mechanisms, the neurotoxic effects of drugs abuse are frequently linked to oxidative stress, mitochondrial malfunction, apoptosis, and suppression of neurogenesis (4) (5). Tramadol is a pain reliever that also has analgesic qualities.…”

Section: Introductionmentioning

confidence: 99%

Prenatal and postnatal development of the rat cerebellar granule cells following maternal administration of thyme and tramadol

Mohamed

Ghait

2022

Zagazig University Medical Journal

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Introduction: Tramadol abuse is increasing among male and female teenagers with a history of substance abuse and anxiety. Many adolescent addicts take tramadol as substitute for other narcotics. Tramadol uptake is associated with many side effects. Thyme has been presumed to have a neuroprotective effect against brain damage. Aim of the work:To assess the harmful effects of tramadol on the pre and postnatal development of the rat cerebellar granule cells and to evaluate the possible ameliorative effect of thyme if being administered with tramadol simultaneously.Material & Methods: Three sets of forty-eight mature female albino rats were randomly organized into three equal groups; control (G1), tramadol treated (G2) and tramadol+thyme treated (G3). After pregnancy, the pregnant rats of each group were categorized into a group designed to be sacrificed at the gestational ages 13 th , 16th and 19 th for the prenatal study. In the other pregnant rat group, their offspring were further subdivided according to their ages into 3 subgroups (newborn, 10 th and 20 th postnatal day) for postnatal evaluation. G1 was not given any treatment. Tramadol HCL (40 mg/Kg/day) dissolved in tab water was given orally to G2. Tramadol (40 mg/Kg/day) and thyme extract (500 mg/kg/day) were given orally to G3. A light, electron microscopic examination and morphometric analysis were performed in the study. Results: By light and electron microscopic examination, there were degenerative and apoptotic changes in the cerebellar cortex of G2. G3 showed improvement in histological changes. Morphometric results showed a decrease in the cerebellar cortex thickness between the G1 and G2 which was significant and an increase in the cerebellar cortex thickness G3 when compared with that of G2. Conclusion:The study assigns that tramadol administration induces adverse effects on the prenatal and postnatal development of the rat cerebellar cortex. It also highlights an improving role of thyme in tramadol-induced cerebellar cortex injury of the pre and postnatal development.

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The role of oxidative stress in toxicities due to drugs of abuse

Cited by 9 publications

References 57 publications

Mitochondria-Related Nuclear Gene Expression in the Nucleus Accumbens and Blood Mitochondrial Copy Number After Developmental Fentanyl Exposure in Adolescent Male and Female C57BL/6 Mice

Mitochondria-Related Nuclear Gene Expression in the Nucleus Accumbens and Blood Mitochondrial Copy Number After Developmental Fentanyl Exposure in Adolescent Male and Female C57BL/6 Mice

An Updated Review on Some Neurotoxic Pharmacological Agents Along with their Neurotoxic Mechanisms

Prenatal and postnatal development of the rat cerebellar granule cells following maternal administration of thyme and tramadol

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