Morphine pre- and post-conditioning exacerbates apoptosis in rat hippocampus cells in a model of homocysteine-induced oxidative stress

Karkhah, Ahmad; Ataee, Ramin; Ataie, Amin

doi:10.3892/br.2017.962

Cited by 16 publications

(6 citation statements)

References 23 publications

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“…It seems that the high dose of BHT, cause injury of the nervous tissue that was appeared in the brain tissue examination in our study which is agreement with Karkhah and et al (22) mention neuropathy led to the effects on the degree of animal interest in the environment has decreased and the length of time required for rotation in the avoidance of the high edge has been increased. Our explanation may be due to the hypothalamic pathway being affected, here is that the neural information follows the slow second pathway from the cerebral cortex to the amygdala, speed of information transmission is slower and takes longer and the response is slower than before (23), represented by delayed in avoid the edge of the slope.…”

Section: Discussionsupporting

confidence: 92%

Toxic effects of butylated hydroxytoluene in rats

Alabdaly¹,

Al-Hamdany²,

Al-Kennany³

2021

IJVS

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This study aimed to assess the acute toxicity in rats of heated and un heatedbutylated hydroxytoluene (BHT). Sunflower oil dissolved BHT, heated at 98±2ºC by a water bath. The animals were divided into five groups. The control group dosage orally with sunflower oil, the first group treated with 250 mg/kg BHT, the second group treated with 250 mg/kg heated, BHT the third group treated with 500 mg/kg BHT and the fourth group treated with 500 mg/kg heated BHT. All groups received oral treatment. The results showed a substantial reduction in motor activity relative to other groups at a dose of 250 mg/kg heated BHT. There was a substantial distinction in the negative geotaxis test in groups of 500 mg/kg heated and un-heated BHT, while a cliff avoidance test in the heat treated dose of 250 and 500 mg/kg was observed in the cliff avoidance test compared to other groups. A significant reduction occurred in all groups in the pocketing and dorsal tonic immobility test. The pathological changes of heated BHT groups were more severe than those of un-heated BHT groups especially the dose of 500 mg/kg heated BHT. It represented by coagulative necrosis, muscle atrophy in heart, interstitial pneumonia, serofibrinous exudate, pulmonary emphysema in lung and neuronal degeneration, microgliosis, myelin vacuolation and satellitosis in the brain. The study concluded that heated BHT at a dose of 250 and 500 mg/kg had toxic effects to motor and neurobehavioral activity, and histopathological changes in the brain, heart, and lung.

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Section: Discussionsupporting

confidence: 92%

Toxic effects of butylated hydroxytoluene in rats

Alabdaly¹,

Al-Hamdany²,

Al-Kennany³

2021

IJVS

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“…This phenomenon was observed in microglial cells and macrophages [ 21 ]. Additionally, many experimental animal studies have shown that morphine increases markers of oxidative stress in the cerebral cortex and serum [ 22 ]. Moreover, significantly increased serum MDA and decreased SOD and CAT activity were observed during tramadol treatment [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Opioid Therapy and Implications for Oxidative Balance: A Clinical Study of Total Oxidative Capacity (TOC) and Total Antioxidative Capacity (TAC)

Kosciuczuk,

Jakubow,

Tarnowska

et al. 2023

JCM

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Background: Opioids are used in pharmacotherapy for chronic pain. The phenomenon of their influence on the oxidative–antioxidant balance is poorly understood. Additionally, little is known about the oxidative status in patients receiving chronic opioid noncancer pain therapy. Methods: The primary goal was to explore oxidative status using the total oxidative capacity (TOC) and total antioxidative capacity (TAC) in patients with chronic lower back pain (LBP) treated with opioids. The secondary task was to present the risk factors connected with the duration of therapy or anthropometric parameters. Plasma TOC and TAC were analyzed in the study group (n = 28), i.e., patients with chronic LBP treated with opioids, and in the control group (n = 11), i.e., healthy volunteers. Results: The TAC was significantly lower in the study group compared to the control group (p < 0.05), while the TOC did not differ significantly. A statistically lower TOC for buprenorphine compared to oxycodone (p = 0.019) and tramadol (p = 0.036) was observed. The TOC did not differ between tramadol and oxycodone. The highest TAC was described for oxycodone, while the TAC for buprenorphine and tramadol was significantly lower in comparison with oxycodone (p = 0.007 and p = 0.016). The TOC/TAC ratio was higher in patients with nicotinism in both groups.Conclusions: Patients receiving chronic opioid therapy presented a lower antioxidative capacity. There were differences in opioid-induced oxidative imbalance, which is very important clinically. Nicotinism increases the oxidative–antioxidative imbalance. The least oxidative capacity was associated with buprenorphine, while oxycodone showed the greatest antioxidant activity. The most favorable TOC/TAC ratio was observed for buprenorphine. It is suggested that buprenorphine or oxycodone has the best profile, and there is no correlation with the duration of opioid therapy or the opioid dose. However, all opioid substances can potentially enhance the oxidative–antioxidative status.

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“…The evidence suggests that parental morphine exposure exacerbates apoptosis and reduces pyramidal neurons in hippocampus (Ghafari and Golalipour, 2014[29]; Karkhah et al, 2017[39]). Another evidence revealed that morphine mediates the physiological changes in the synaptic plasticity in the hippocampus (Sarkaki et al, 2008[60]).…”

Section: Discussionmentioning

confidence: 99%