Evaluation of the protective effect of coenzyme Q10 on hepatotoxicity caused by acute phosphine poisoning.

Background: Aluminum phosphide (AlP) poisoning is prevalent in numerous countries, resulting in high mortality rates. Phosphine gas, the primary agent responsible for AlP poisoning, exerts detrimental effects on various organs, notably the heart, liver and kidneys. Numerous studies have documented the advantageous impact of Coenzyme Q10 (CoQ10) in mitigating hepatic injuries. The objective of this investigation is to explore the potential protective efficacy of CoQ10 against hepatic toxicity arising from AlP poisoning. Method: The study encompassed distinct groups receiving almond oil, normal saline, exclusive CoQ10 (at a dosage of 100 mg/kg), AlP at 12 mg/kg; LD50 (lethal dose for 50%), and four groups subjected to AlP along with CoQ10 administration (post-AlP gavage). CoQ10 was administered at 10, 50, and 100 mg/kg doses via Intraparietal (ip) injections. After 24 h, liver tissue specimens were scrutinized for mitochondrial complex activities, oxidative stress parameters, and apoptosis as well as biomarkers such as aspartate transaminase (AST) and alanine transaminase (ALT). Results: AlP induced a significant decrease in the activity of mitochondrial complexes I and IV, as well as a reduction in catalase activity, Ferric Reducing Antioxidant Power (FRAP), and Thiol levels. Additionally, AlP significantly elevated oxidative stress levels, indicated by elevated reactive oxygen species (ROS) production, and resulted in the increment of hepatic biomarkers such as AST and ALT. Administration of CoQ10 led to a substantial improvement in the aforementioned biochemical markers. Furthermore, phosphine exposure resulted in a significant reduction in viable hepatocytes and an increase in apoptosis. Co-treatment with CoQ10 exhibited a dose-dependent reversal of these observed alterations. Conclusion: CoQ10 preserved mitochondrial function, consequently mitigating oxidative damage. This preventive action impeded the progression of heart cells toward apoptosis.

Carboxymethyl chitosan-alginate hydrogel containing GSNO with the ability to nitric oxide release for diabetic wound healing.

Despite significant progress in developing diabetic wound dressing, the fabrication of an ideal one that fulfills all virtual criteria, such as promoting angiogenesis, is still lacking. Given the low vascularization in chronic diabetic wounds, they have a severe and non-healing nature. In this study, Nitric oxide (NO) was used as an angiogenic agent, which also has antibacterial properties. Briefly, S-nitrosoglutathione (GSNO) as a NO-donor was physically loaded into the carboxymethyl chitosan (CMC)/sodium alginate (ALg) composite film (CMC-ALg-GSNO). The morphological evaluation via scanning electron microscope confirms the homogeneous and porous structure of the wound dressing. The water uptake and water vapor transmission for the wound dressing were 4354.1% ± 179.3% and 2753.8 ± 54.6 g m-2per day, respectively. Anin-vitrorelease study showed a continuous delivery of NO during 168 h. Besides, the result from thein-vivotest reveals that the CMC-ALg-GSNO wound dressing developed diabetic wound healing in a rat model compared to the CMC-ALg and gauze. Thus, this study showed that CMC-ALg-GSNO wound dressing could lead to novel therapeutic invasions to treat diabetic wounds.

Evaluation of anesthesia quality with three methods: "propofol + fentanyl" vs. "propofol + fentanyl + lidocaine" vs. "propofol + fentanyl + lidocaine + ketamine" in patients referred to the scoping ward.

Introduction: Toleration of the complexity and pain of interventions such as endoscopy and colonoscopy is highly difficult for patients. Considering the disagreement on the method of injection of propofol, this study was performed to evaluate the quality of anesthesia using the three methods of propofol + fentanyl, propofol + fentanyl + lidocaine, and propofol + fentanyl + lidocaine + ketamine. Methods: This one-way blind clinical trial study included 99 patients who were admitted in three groups by block randomization method. In a group of patients that were sedated with propofol + fentanyl + lidocaine + ketamine, the dose of all drugs is reduced by half the amount of the other groups. Variables included age, sex, frequency of cough, apnea, need for jaw thrust maneuver, O2 saturation, duration of recovery, and procedural satisfaction. Data were analyzed using SPSS version 20.0. P value of < 0.05 was considered to be significant. Results: The three groups were similar in terms of demographic characteristics. The effects of the three sedation protocols on the variables showed that patient's apnea, cough, O2 saturation, and also proceduralist satisfaction in the group of the patient that sedated with four drugs was significantly higher (P < 0.05) than other groups. But there was no significant difference between the three groups when comparing the recovery time and need for jaw thrust during the procedure. Conclusion: The findings of the present study showed that the use of combination of "propofol + fentanyl + lidocaine + ketamine" with lower doses, significantly results in higher quality sedation compared with higher doses of "propofol + fentanyl + lidocaine" or "propofol + fentanyl" for scoping procedures.

Potential prognostic roles of serum lactate and Creatine kinase levels in poisoned patients.

BACKGROUND: Examination of serum lactate level and its changes, as an indicator of tissue oxygenation, as well as level of creatine kinase (CK) inhibitors, as a factor of mortality which partially expresses heart, brain, and muscle damage, may be considered as tools to determine prognosis in critically ill patients. We aimed to evaluate these two factors as potential prognostic factors in critically poisoned patients admitted to our toxicology ICU. METHOD: This is a cross-sectional descriptive-analytic study that was performed on poisoned patients referred to emergency department of Loghman Hakim Hospital. One-hundred critically poisoned patients who had been admitted to ICU were conveniently chosen using a random number table and included into the study after obtaining consent forms from their next of kin. Their serum lactate and CK levels were checked on admission. These levels were compared subsequently between survivors and non-survivors to seek for their potential prognostic role. RESULTS: In a total of 100 patients enrolled, 61 were male. Serum level of lactate (with a cut off of 26 mg/dL) and serum CK with a cutoff point of 169 U/L could have prognosticated death with sensitivity and specificity of 78 and 77% (for lactate) and 74 and 62% (for serum CK), respectively. CONCLUSIONS: In poisoned patients, serum lactate and CK can be used as possible prognostic factors because they rapidly increase in the serum and are easily detectable.

Neuroprotective effects of lipopolysaccharide and naltrexone co­preconditioning in the photothrombotic model of unilateral selective hippocampal ischemia in rat.

Preconditioning with lipopolysaccharide (LPS) or opioid antagonists has a neuroprotective effect in ischemic insults. However, the co­preconditioning effect of toll­like receptor ligands and opioid antagonists has not been investigated. In this study we examined the neuroprotective effect of LPS and naltrexone (NTX) preconditioning and co­preconditioning in unilateral selective hippocampal ischemia in rats to assess for possible synergistic protective effects. LPS and NTX were injected unilaterally into the left cerebral ventricle of male rats. Forty­eight hours after LPS and twenty­four hours after NTX injection, ipsilateral selective hippocampal ischemia was induced using a modified version of the photothrombotic method. Protective effects for LPS and NTX were assessed by evaluating infarct volume (using 2,3,5­triphenyltetrazolium chloride staining), and cognitive function (using radial arm water maze and passive avoidance tests). Animals in the ischemic group had an infarct lesion and considerable cognitive impairment, compared with the sham group. LPS or NTX preconditioning significantly reduced the infarct size and improved cognitive function. Moreover, co­preconditioning with LPS and NTX increased the protective effect compared with preconditioning with LPS or NTX alone. Our data showed that LPS and NTX preconditioning resulted in a neuroprotective effect in hippocampal ischemia. Furthermore, co­preconditioning with LPS and NTX resulted in a synergistic protective effect.

Molecular and biochemical evidence on the protection of cardiomyocytes from phosphine-induced oxidative stress, mitochondrial dysfunction and apoptosis by acetyl-L-carnitine.

The aim of the present study was to investigate the efficacy of acetyl-L-carnitine (ALCAR) on pathologic changes of mitochondrial respiratory chain activity, ATP production, oxidative stress, and cellular apoptosis/necrosis induced by aluminum phosphide (AlP) poisoning. The study groups included: the Sham that received almond oil only; the AlP that received oral LD50 dose of aluminum; the AC-100, AC-200, and AC-300 which received concurrent oral LD50 dose of AlP and single 100, 200, and 300 mg/kg of ALCAR by intraperitoneal injection. After 24 h, the rats were sacrificed; the heart and blood sample were taken for measurement of biochemical and mitochondrial factors. The results specified that ALCAR significantly attenuated the oxidative stress (elevated ROS and plasma iron levels) caused by AlP poisoning. ALCAR also increased the activity of cytochrome oxidase, which in turn amplified ATP production. Furthermore, flow cytometric assays and caspase activity indicated that ALCAR prohibited AlP-induced apoptosis in cardiomyocytes.