المؤلفون: Khadrawy, Yasser A., Hosny, Eman N., El-Gizawy, Mayada M., Sawie, Hussein G., Aboul Ezz, Heba S.

المصدر: Cardiovascular Toxicology; Jun2021, Vol. 21 Issue 6, p433-443, 11p

مصطلحات موضوعية: CURCUMIN, TUMOR necrosis factors, LABORATORY rats, CISPLATIN, CARDIOTOXICITY, ACETYLCHOLINESTERASE, LACTATE dehydrogenase

مستخلص: The cardiotoxicity of chemotherapeutic drugs as cisplatin has become a major issue in recent years. The present study investigates the efficacy of curcumin nanoparticles against the cardiotoxic effects of cisplatin by assessment of oxidative stress parameters, Na⁺,K⁺-ATPase, acetylcholinesterase (AchE) and tumor necrosis factor-alpha (TNF-α) in cardiac tissue in addition to serum lactate dehydrogenase (LDH). Rats were divided into three groups: control rats that received saline for 14 days; cisplatin-treated rats that received a single intraperitoneal (i.p.) injection of cisplatin (12 mg/kg) followed by a daily oral administration of saline (0.9%) for 14 days and rats treated with a single i.p. injection of cisplatin (12 mg/kg) followed by a daily oral administration of curcumin nanoparticles (50 mg/kg) for 14 days. Cisplatin resulted in a significant increase in lipid peroxidation, nitric oxide (NO), and TNF-α and a significant decrease in reduced glutathione (GSH) levels and Na⁺, K⁺- ATPase activity. Moreover, significant increases in cardiac AchE and serum lactate dehydrogenase activities were recorded. Treatment of cisplatin-injected animals with curcumin nanoparticles ameliorated all the alterations induced by cisplatin in the heart of rats. This suggests that curcumin nanoparticles can be used as an important therapeutic adjuvant in chemotherapeutic and other toxicities mediated by oxidative stress and inflammation. [ABSTRACT FROM AUTHOR]

: Copyright of Cardiovascular Toxicology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Akintunde, J. K., Oyedibu, G. O., Olanipekun, N. J., Olaleye, O. A.

المصدر: Cardiovascular Toxicology; Apr2021, Vol. 21 Issue 4, p272-285, 14p

مصطلحات موضوعية: OXIDATIVE stress, LACTATE dehydrogenase, CHRONIC toxicity testing, CARDIOVASCULAR diseases, GLUTATHIONE, SUPEROXIDE dismutase

مستخلص: Chronic mixed toxicant exposure has been implicated in the aetiology of lung and heart failure through prolonged free radical generations. This study was carried out to assess the protective effect of naturally occurring phenolic components from Croton zambesicus (400 mg/kg C-ZAMB) leaves against cardiopulmonary toxicity induced by chronic mixed toxicant (0.5 mL EOMABRSL) in rats. Chronic cardiopulmonary injury via oral administration of 0.5 ml EOMABRSL for 98 days (non-withdrawal) and 70 days (withdrawal) caused unhealthy alteration in the levels of oxidative stress biomarkers [malondialdehyde (MDA), reduced glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase]. Similarly, both withdrawal and non-withdrawal approaches of EOMABRSL-exposed animals exhibited increase in the activity of eco-5¹-nucleotidase (5¹ENT) with corresponding diminution in the activity of lactate dehydrogenase (LDH), i.e. the metabolic fuel for cardiopulmonary wellness. Ultimately, histology examination confirmed hyperplastic, bronchopneumonia and cloudy swelling of cardiovascular cells followed by the accumulation of cellular exudates and haemorrhage in the alveoli and bronchioles. The active antioxidants of 400 mg/kg C-ZAMB leaves were responsible for the biological protection of cardiopulmonary toxicity by modulating the activities of 5¹ENT and LDH. The oxidative stress was also reversed by 400 mg/kg phenolic C-ZAMB leaves in the heart and lungs. Hence, 400 mg/kg phenolic C-ZAMB leaves may be a natural therapy for the treatment of cardiovascular disorder associated with pulmonary dysfunction in rats. [ABSTRACT FROM AUTHOR]

: Copyright of Cardiovascular Toxicology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Kale, Oluwafemi Ezekiel, Gündüz, Miyase Gözde, Ogunbiyi, Babafemi Tosin, Ogundare, Temitope Funmi, Ekor, Martins, Awodele, Olufunsho

المصدر: Cardiovascular Toxicology; Dec2020, Vol. 20 Issue 6, p627-640, 14p

مصطلحات موضوعية: CALCIUM antagonists, TUMOR necrosis factors, CALCIUM channels, RATS, LACTATE dehydrogenase, ALANINE aminotransferase, ALANINE

مستخلص: Recent evidence indicates that Ca²⁺ dysregulation is involved in the pathogenesis of isoproterenol (ISP)-induced biochemical toxicity and associated oxidative stress. In this study, we investigated the chemopreventive benefit of M3, a 1,4-dihydropyridine calcium channel blocker, against ISP-induced toxicity in male Wistar rats. Adult rats were divided into eight groups of six rats/group. Groups 1–5 received normal saline (control, 10 mL/kg/day, p.o.), ISP (85 mg/kg/day, s.c.), M3 lower dose (M3LD, 5 mg/kg, p.o.), M3 upper dose (M3UD, 20 mg/kg/day, p.o.), and Nifedipine (NFD, 20 mg/kg/day, p.o.), respectively. Others (groups 6–8) were pretreated with either M3LD, M3UD or NFD one hour before ISP administration. All rats were sacrificed 24 h after the last administration and changes in biochemical, hematological, and antioxidant parameters were assessed. Histologic examination of the heart, liver and kidney was also conducted. ISP elevated (p < 0.05) Ca²⁺, alanine aminotransferase, lactate dehydrogenase, triglycerides, and low-density lipoprotein levels when compared with control. Similarly, ISP increased levels of markers of renal function (p < 0.01), C-reactive protein (148.1%) and myocardial malondialdehyde (MDA, 88.7%) and tumor necrosis factor-alpha (109.2%). Platelet level was reduced (p < 0.05) in the ISP-intoxicated control rats. M3 exhibited antioxidant property, reduced levels of triglycerides, MDA and improved biochemical and hematological alterations associated with ISP toxicity. M3, however, was not effective in restoring histological changes that characterized ISP toxicity at the doses used. M3 offers chemopreventive benefits against ISP toxicity possibly through L-/T-type calcium channels blockade and modulatory actions on biochemical and antioxidant homeostasis. [ABSTRACT FROM AUTHOR]

: Copyright of Cardiovascular Toxicology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Botelho, Ana F. M., Miranda, Ana L. S., Freitas, Thalita G., Milani, Paula F., Barreto, Tatiane, Cruz, Jáder S., Melo, Marília M.

المصدر: Cardiovascular Toxicology; Dec2020, Vol. 20 Issue 6, p539-547, 9p

مصطلحات موضوعية: DIGOXIN, OUABAIN, LACTATE dehydrogenase, WESTERN immunoblotting, TROPONIN I, PHYSIOLOGY education

مستخلص: The aim of this study was to evaluate the comparative effects of CGs on heart physiology. Twenty-eight Wistar rats were distributed into four groups (n = 7), control group received NaCl 0.9% every 24 h for 21 days; treated groups received respectively 50 μg/kg of digoxin (DIG), ouabain (OUA) and oleandrin (OLE) every 24 h for 21 days. Serial ECGs were performed, as well as serum levels of creatinine kinase (CK), its MB fraction, troponin I (cTnI), calcium (Ca²⁺) and lactic dehydrogenase (LDH). Heart tissue was processed for histology, scanning electron microscopy and Western blot analysis for cTnI, brain natriuretic peptide (BNP), sodium potassium pump alpha-1 and alpha-2. Ventricle samples were also analyzed for thiobarbituric acid reactive substances and antioxidant enzymes (SOD, GPX, and CAT). ECGs showed decrease in QT and progressive shortening of QRS. No arrhythmias were observed. No significant differences were associated with CGs treatment and serum levels of CK, CK-MB, and cTnI. Only oleandrin increased LDH levels. Histological analysis showed degenerative changes and only oleandrin promoted moderate focal necrosis of cardiomyocytes. Scanning microscopy also confirmed the greatest effect of oleandrin, with rupture and shortening of cardiac fibers. The expression of troponin I and alpha-1 isoform were not altered, however, the protein levels of BNP and alpha-2 were higher in the groups that received oleandrin and ouabain in relation to the digoxin group. All GCs affected the production of ROS, without causing lipid peroxidation, through the activation of different antioxidant pathways. It is concluded that the administration of digoxin, ouabain, and oleandrin at 50 µg/kg for 21 days caused cardiovascular damage that represent an important limitation into its future use in heart failure and antineoplastic therapy. [ABSTRACT FROM AUTHOR]

: Copyright of Cardiovascular Toxicology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Yan, Yi, Xiang, Chengyu, Yang, Zhijian, Miao, Dengshun, Zhang, Dingguo

المصدر: Cardiovascular Toxicology; Aug2020, Vol. 20 Issue 4, p351-360, 10p

مصطلحات موضوعية: HEART injuries, VENTRICULAR ejection fraction, LACTATE dehydrogenase, CREATINE kinase, CELLULAR aging

مستخلص: Adriamycin (ADR)-induced chronic heart injury (CHI) is a serious complication of chemotherapy. The present study was designed to assess the ability of fasudil, a Rho kinase inhibitor, to prevent ADR-induced CHI. Forty male 6-week-old C57BL6 mice were randomly divided into the following four groups: (1) control group, (2) CHI induced by adriamycin (ADR group), (3) CHI plus low dose fasudil (ADR + L group), and (4) CHI plus high dose fasudil (ADR + H group). Animals from groups 2–4 received ADR (2.5 mg/kg, i.p.) once a week for 8 weeks, and the control group received saline. Meanwhile, the animals in groups 3–4 received 2 mg/kg/day or 10 mg/kg/day fasudil, respectively. After measurement of cardiac functions, blood samples were collected for biochemical assays. The hearts were excised for histological, immunohistochemistry and western blot study, respectively. Adriamycin produced evident cardiac damage revealed by cardiac functions changes: decreased left ventricular fractional shortening (FS), left ventricular ejection fraction (EF), increased left ventricular volume, cardiac injury marker changes (increased creatine kinase, lactate dehydrogenase), antioxidant enzymes activity changes (decreased superoxide dismutase), and lipid peroxidation (elevated malondialdehyde) to the control group. Fasudil treatment notably ameliorated ADR-induced cardiac damage, restored heart function, suppressed cell apoptosis and senescence, ameliorated redox imbalance, and DNA damage. Fasudil has a protective effect on ADR-induced chronic heart injury, which partially attributed to its antioxidant, anti-apoptotic effects of inhibiting the RhoA/Rho kinase (ROCK) signaling pathway. [ABSTRACT FROM AUTHOR]

: Copyright of Cardiovascular Toxicology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Ahmed, Nishat, El-Agamy, Dina Saad, Mohammed, Gamal Abdallah, Abo-Haded, Hany, Elkablawy, Mohamed, Ibrahim, Sabrin Ragab Mohamed

المصدر: Cardiovascular Toxicology; Apr2020, Vol. 20 Issue 2, p121-129, 9p

مصطلحات موضوعية: TROPONIN I, ALKALINE phosphatase, OXIDANT status, LACTATE dehydrogenase, LIPOPOLYSACCHARIDES, DIETARY supplements, OXIDATIVE stress

مستخلص: Recently, there is an increasing interest in searching for harmless natural products isolated from plant materials that can be used as beneficial dietary supplements and/or therapeutic drug candidates. The present study aimed to test the potential protective role of Pulicaria petiolaris (PP, Asteraceae) against hepatic and cardiotoxic effects associated with lipopolysaccharide (LPS) injection. PP was given orally for 5 days at two different doses before LPS injection. Results have shown that LPS induced remarkable hepatic and cardiac injurious effects in mice. Hepatic damage was evident through increased serum transaminases, lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and activity. Estimation of high levels of serum creatine kinase-MB (CK-MB) and cardiac troponin I indicated cardiac damage. Histopathological examination of liver and heart confirmed the biochemical results. Increase in oxidative stress along with a depressed antioxidant status of liver and heart were observed in LPS-intoxicated animals. Furthermore, LPS induced activation of nuclear factor-κB (NF-κB) and subsequent elevation of inflammatory cytokines (TNF-α, IL-6). On the other hand, PP treatment successfully safeguards both organs against LPS-induced injury as indicated by the improvement of the biochemical and histopathological parameters. These results suggest that PP ameliorates LPS-induced hepatic and cardiac oxidative injurious effects via antioxidant and anti-inflammatory effects. [ABSTRACT FROM AUTHOR]

: Copyright of Cardiovascular Toxicology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Rustem Anil Ugan, Muhammed Yayla, Hamza Halici, Pinar Bayram, Taha Tavaci, Irfan Cinar, Erdem Toktay

المصدر: Cardiovascular toxicology. 22(1)

مصطلحات موضوعية: Male, Anti-Inflammatory Agents, Myocardial Infarction, Apoptosis, Pharmacology, Toxicology, medicine.disease_cause, Antioxidants, Cell Line, Superoxide dismutase, chemistry.chemical_compound, In vivo, Lactate dehydrogenase, medicine, Animals, Myocytes, Cardiac, Viability assay, Molecular Biology, Flavonoids, Mice, Inbred BALB C, biology, Chemistry, Isoproterenol, Glutathione, Malondialdehyde, Cardiotoxicity, Rats, Disease Models, Animal, Oxidative Stress, biology.protein, Cytokines, Inflammation Mediators, Cardiology and Cardiovascular Medicine, Apoptosis Regulatory Proteins, Oxidative stress

الوصف: The aim of the study was to examine the protective effects and possible mechanism of gossypin against isoproterenol (ISO)-mediated myocardial damage in vivo and H9c2 cell damage in vitro. H9c2 cells were categorized into five groups. Viability was evaluated with MTT and LDH release in H9c2 cells. Apoptotic parameter analysis was performed with cytochrome c (Cyt-c), caspase-3 (CASP-3), and BCL2/Bax mRNA expression levels. In vivo, gossypin was administered orally to mice at doses of 5, 10, and 20 mg/kg for 7 days. ISO groups were injected with isoproterenol (150 mg/kg) subcutaneously (on 8th and 9th) for 2 days. Afterward, lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB) levels and Troponin-I (Tn-I) amount from their serum, oxidative stress parameters superoxide dismutase (SOD) activity, glutathione (GSH) and malondialdehyde (MDA) levels, and tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1 β), and NF-kB mRNA expression levels with inflammatory markers from heart tissue were evaluated. In addition, IL-1B, BCL-2, and cas-3 immunohistochemical staining was performed from heart tissue and TNF-a level was measured by ELISA method. Administration of Gossypin protected the cells by dose-dependent, eliminating the reduced cell viability and increased LDH release of ISO in H9c2 cells. In mice serum analyses, increased LDH, CK-MB levels, and Tn-I levels were normalized by gossypin. ISO administration in heart tissue is regulated by gossypin with increased SOD activity, GSH amount, TNF-α, IL-6, IL-1β, and NF-kB mRNA expression levels and decreased MDA amount. Overall, the present results demonstrated that gossypin has a potential cardioprotective treatment for ischemic heart disease on in vivo and in vitro.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a325d3eedee62bca500dfae487169334Test
https://pubmed.ncbi.nlm.nih.gov/34599475Test

المؤلفون: Gamal Abdallah Mohammed, Mohamed A. Elkablawy, Sabrin R.M. Ibrahim, Dina S. El-Agamy, Nishat Ahmed, Hany M. Abo-Haded

المصدر: Cardiovascular Toxicology. 20:121-129

مصطلحات موضوعية: Lipopolysaccharides, Male, Antioxidant, Heart Diseases, Lipopolysaccharide, medicine.medical_treatment, Anti-Inflammatory Agents, 030204 cardiovascular system & hematology, Pharmacology, Toxicology, medicine.disease_cause, Antioxidants, Pulicaria, Proinflammatory cytokine, Mice, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Lactate dehydrogenase, medicine, Animals, Molecular Biology, Cardiotoxicity, biology, Interleukin-6, Plant Extracts, Tumor Necrosis Factor-alpha, Myocardium, NF-kappa B, biology.organism_classification, Disease Models, Animal, Oxidative Stress, Liver, chemistry, 030220 oncology & carcinogenesis, Alkaline phosphatase, Lipid Peroxidation, Chemical and Drug Induced Liver Injury, Cardiology and Cardiovascular Medicine, Oxidative stress, Signal Transduction

الوصف: Recently, there is an increasing interest in searching for harmless natural products isolated from plant materials that can be used as beneficial dietary supplements and/or therapeutic drug candidates. The present study aimed to test the potential protective role of Pulicaria petiolaris (PP, Asteraceae) against hepatic and cardiotoxic effects associated with lipopolysaccharide (LPS) injection. PP was given orally for 5 days at two different doses before LPS injection. Results have shown that LPS induced remarkable hepatic and cardiac injurious effects in mice. Hepatic damage was evident through increased serum transaminases, lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and activity. Estimation of high levels of serum creatine kinase-MB (CK-MB) and cardiac troponin I indicated cardiac damage. Histopathological examination of liver and heart confirmed the biochemical results. Increase in oxidative stress along with a depressed antioxidant status of liver and heart were observed in LPS-intoxicated animals. Furthermore, LPS induced activation of nuclear factor-κB (NF-κB) and subsequent elevation of inflammatory cytokines (TNF-α, IL-6). On the other hand, PP treatment successfully safeguards both organs against LPS-induced injury as indicated by the improvement of the biochemical and histopathological parameters. These results suggest that PP ameliorates LPS-induced hepatic and cardiac oxidative injurious effects via antioxidant and anti-inflammatory effects.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5a140eb1efe95f580e352bca90a05516Test
https://doi.org/10.1007/s12012-019-09539-4Test

المؤلفون: Azza A.K. El-Sheikh, Zenat A. Khired

المصدر: Cardiovascular toxicology. 21(7)

مصطلحات موضوعية: Male, Heart Diseases, Antineoplastic Agents, Apoptosis, Breast Neoplasms, 030204 cardiovascular system & hematology, Pharmacology, Toxicology, medicine.disease_cause, Superoxide dismutase, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Lactate dehydrogenase, medicine, Animals, Humans, Drug Interactions, Myocytes, Cardiac, Rats, Wistar, Molecular Biology, Cisplatin, Cardiotoxicity, biology, Dose-Response Relationship, Drug, Morphine, Caspase 3, Malondialdehyde, Analgesics, Opioid, Disease Models, Animal, Oxidative Stress, MCF-7, chemistry, Drug Resistance, Neoplasm, 030220 oncology & carcinogenesis, Cancer cell, biology.protein, MCF-7 Cells, Cytokines, Female, Lipid Peroxidation, Inflammation Mediators, Cardiology and Cardiovascular Medicine, Oxidative stress, medicine.drug

الوصف: Morphine (MOR) is a strong analgesic that is often used in treatment of severe pains during cancer treatment, and thus might be concomitantly used with anticancer drugs as cisplatin (CP). The aim of the current study was to investigate the mechanisms by which MOR can affect CP-induced cardiotoxicity and to explore effects of MOR on the cytotoxic efficacy of CP. MOR (10 mg/kg/day i.p.) was administered to rats for 10 days, with or without 7.5 mg/kg CP single i.p. dose at day 5 of the experiment. In addition, MOR and/or CP were administered to MCF-7 cells to test their cytotoxicity. Compared to control, CP caused cardiotoxic effects manifested by significant increase in serum enzymatic markers; creatine kinase-MB and lactate dehydrogenase, with histopathological cardiac damage. In addition, CP caused cardiac oxidative stress, manifested by significant increased tissue lipid peroxidation product; malondialdehyde and nitric oxide, with significant decrease in tissue antioxidants as reduced glutathione, superoxide dismutase and catalase compared to control. Furthermore, CP significantly increased tissue proinflammatory cytokines; TNF-α and IL-6, as well as upregulated the apoptotic marker; caspase 3 compared to control. MOR/CP combination significantly deteriorated all tested parameters compared to CP alone. In MCF-7 breast cancer cells, administration of MOR in concentrations of 0.1, 1, 10 or 30 μM concomitantly with 1 or 10 μM CP caused dose-dependent reduction in CP-induced cytotoxicity in vitro. In conclusion, MOR administration might deteriorate CP-induced cardiotoxicity during cancer chemotherapy through oxidant, pro-inflammatory and apoptotic mechanisms, and might reduce CP chemotherapeutic efficacy.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f2b5a45d3b577a6b24cd25120ad30cc7Test
https://pubmed.ncbi.nlm.nih.gov/33796943Test

المؤلفون: J K Akintunde, O A Olaleye, N J Olanipekun, G O Oyedibu

المصدر: Cardiovascular toxicology. 21(4)

مصطلحات موضوعية: Lung Diseases, Heart Diseases, 030204 cardiovascular system & hematology, Pharmacology, Toxicology, medicine.disease_cause, Antioxidants, Superoxide dismutase, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Phenols, Lactate dehydrogenase, medicine, Animals, Rats, Wistar, Molecular Biology, Lung, biology, Myocardium, Heart, Glutathione, Malondialdehyde, Cardiotoxicity, Plant Leaves, Oxidative Stress, chemistry, Catalase, 030220 oncology & carcinogenesis, Toxicity, biology.protein, Environmental Pollutants, Female, Croton, Cardiology and Cardiovascular Medicine, Oxidative stress, Biomarkers, Toxicant

الوصف: Chronic mixed toxicant exposure has been implicated in the aetiology of lung and heart failure through prolonged free radical generations. This study was carried out to assess the protective effect of naturally occurring phenolic components from Croton zambesicus (400 mg/kg C-ZAMB) leaves against cardiopulmonary toxicity induced by chronic mixed toxicant (0.5 mL EOMABRSL) in rats. Chronic cardiopulmonary injury via oral administration of 0.5 ml EOMABRSL for 98 days (non-withdrawal) and 70 days (withdrawal) caused unhealthy alteration in the levels of oxidative stress biomarkers [malondialdehyde (MDA), reduced glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase]. Similarly, both withdrawal and non-withdrawal approaches of EOMABRSL-exposed animals exhibited increase in the activity of eco-51-nucleotidase (51ENT) with corresponding diminution in the activity of lactate dehydrogenase (LDH), i.e. the metabolic fuel for cardiopulmonary wellness. Ultimately, histology examination confirmed hyperplastic, bronchopneumonia and cloudy swelling of cardiovascular cells followed by the accumulation of cellular exudates and haemorrhage in the alveoli and bronchioles. The active antioxidants of 400 mg/kg C-ZAMB leaves were responsible for the biological protection of cardiopulmonary toxicity by modulating the activities of 51ENT and LDH. The oxidative stress was also reversed by 400 mg/kg phenolic C-ZAMB leaves in the heart and lungs. Hence, 400 mg/kg phenolic C-ZAMB leaves may be a natural therapy for the treatment of cardiovascular disorder associated with pulmonary dysfunction in rats.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::93e2af143d4e4aaee7811cc960ad490eTest
https://pubmed.ncbi.nlm.nih.gov/33135141Test