Displaying publications 1 - 20 of 27 in total

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  1. Marzilawati AR, Ngau YY, Mahadeva S
    PMID: 23021009 DOI: 10.1186/2050-6511-13-8
    The metabolism of paracetamol in Asians is thought to differ from Westerners. Detailed clinical features of paracetamol -induced hepatotoxicity among Asians remains largely unreported.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology*
  2. Fauzi ARM, Shah A, Rathor MY, Satwi S
    Med J Malaysia, 2004 Mar;59(1):72-7.
    PMID: 15535339
    A prospective survey on 14 consecutive cases with tuberculous drug induced hepatitis was done at our chest clinic in a state general hospital over a period of 15 months. There were 30 controls chosen randomly from the chest clinic register. The cases had lower mean body mass index (P<0.008), serum albumin (P<0.005) and higher serum globulin (P<0.04). Serum liver transaminases and total bilirubin rose significantly during the acute episode of drug induced hepatitis. Among the risk factors studied, only chronic hepatitis B carrier status was found to be more prevalent among the cases. There was one death (7.1%) over the whole study period.
    Study site: Chest clinic, Hospital Tengku Ampuan Afzan (HTAA), Kuantan, Pahang, Malaysia
    Matched MeSH terms: Drug-Induced Liver Injury/etiology*
  3. Jayalakshmi P, Ting HC
    Histopathology, 1990 Jul;17(1):89-91.
    PMID: 2146206
    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  4. Chan KW, Cheong IKS
    Med J Malaysia, 1982 Sep;37(3):227-30.
    PMID: 7177004
    There is evidence to show that paraquat poisoning is alarmingly common in Malaysia. This paper reviews 30 cases of paraquat poisoning seen at the General Hospital, Kuala Lumpur from 1978 to 1979 inclusive. Preventive measures and management are discussed. It is felt that tighter legislation to control its use in agriculture should be implemented now.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  5. Giam YC, Tham SN, Tan T, Lim A
    Ann Acad Med Singap, 1986 Jan;15(1):118-21.
    PMID: 2939787
    Drug eruptions from indeginous medicine is often difficult to diagnosis and confirm. It is known that a number of these now supplied by bomohs and Chinese sinsehs contain known drugs and are dispensed as tablets and capsules. We report 3 cases of adverse drug eruption to "Jamu", a Malay herb. A particular brand, "Jamu Indonesia, Toko Air Pancur", from Johor Bahru, Malaysia, is especially recommended for "sakit pinggang" or backache. The cases occurred between January and February 1985, and all had taken brown kidney shaped tablets. The adverse reactions were moderately severe. Two had erythroderma with hepatitis, and one, Steven Johnson Syndrome. Analysis of this jamu for analgesics led to the discovery of adulteration with phenylbutazone and diazepam. Records from local cases from 1974-1984 showed that 8 other patients, all Chinese had adverse cutaneous eruptions from phenylbutazone, oxybutazone and propyphenazone. The skin manifestations were erythroderma (2 cases), vasculitis (2 cases) and toxic epidermal necrolysis (4 cases). Those with toxic epidermal necrolysis had 100% mortality.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  6. Nassar I, Pasupati T, Judson JP, Segarra I
    Malays J Pathol, 2010 Jun;32(1):1-11.
    PMID: 20614720 MyJurnal
    Imatinib, a selective tyrosine kinase inhibitor, is the first line treatment against chronic myelogenous leukaemia (CML) and gastrointestinal stromal tumors (GIST). Several fatal cases have been associated with imatinib hepatotoxicity. Acetaminophen, an over-the-counter analgesic, anti-pyretic drug, which can cause hepatotoxicity, is commonly used in cancer pain management. We assessed renal and hepatic toxicity after imatinib and acetaminophen co-administration in a preclinical model. Four groups of male ICR mice (30-35 g) were fasted overnight and administered either saline solution orally (baseline control), imatinib 100 mg/kg orally (control), acetaminophen 700 mg/kg intraperitoneally (positive control) or co-administered imatinib 100 mg/kg orally and acetaminophen 700 mg/kg intraperitoneally (study group), and sacrificed at 15 min, 30 min, 1 h, 2 h, 4 h and 6 h post-administration (n = 4 per time point). The liver and kidneys were harvested for histopathology assessment. The liver showed reversible cell damage like feathery degeneration, microvesicular fatty change, sinusoidal congestion and pyknosis, when imatinib or acetaminophen were administered separately. The damage increased gradually with time, peaked at 2 h but resolved by 4 h. When both drugs were administered concurrently, the liver showed irreversible damage (cytolysis, karyolysis and karyorrhexis) which did not resolve by 6 h. Very minor renal changes were observed. Acetaminophen and imatinib co-administration increased hepatoxicity which become irreversible, probably due to shared P450 biotransformation pathways and transporters in the liver.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  7. Vakiloddin S, Fuloria N, Fuloria S, Dhanaraj SA, Balaji K, Karupiah S
    Pak J Pharm Sci, 2015 May;28(3):951-7.
    PMID: 26004728
    The objective of present study was to explore the hepatoprotective and antioxidant profile of Citrullus colocynthis fruits. Hepatoprotective profile of methanolic extract of Citrullus colocynthis fruits (MECCF) was investigated on rats, which were made hepatotoxic using paracetamol. The antioxidant profile of MECCF was evaluated by conducting Catalase, Super oxide Dismutase, Lipid Peroxidation and Diphenyl Picryl Hydrazyl tests. During hepatoprotective investigation, the Paracetamol treated group II showed significant increase in total bilirubin (TB), serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) and alkaline phosphatase (ALP) level. The results so obtained showed that pretreatment of rats with MECCF 300mg/kg p.o. decreases the elevated TB, SGOT, SGPT and ALP serum levels. Also, MECCF inhibitory profile was found comparable with toxicant group (Paracetamol 2g/kg, p.o.). The present study concludes that MECCF fruit possess significant hepatoprotective and antioxidant activity.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology*
  8. Sasidharan S, Aravindran S, Latha LY, Vijenthi R, Saravanan D, Amutha S
    Molecules, 2010 Jun 23;15(6):4478-89.
    PMID: 20657455 DOI: 10.3390/molecules15064478
    BACKGROUND: The objective of this study was to investigate the antioxidant and hepatoprotective effects of methanolic extracts of L. edodes and the determination of their total phenolics content.

    RESULTS: The amount of total phenolics was estimated to be 70.83 mg Gallic Acid Equivalent (GAE) per gram of dry extract. The antioxidant activity of the L. edodes extract was 39.0% at a concentration of 1 mg/mL and was also concentration dependant, with an EC(50) value of 4.4 mg/mL. Different groups of animals (Wister albino mice) were administered paracetamol (1 g/kg, p.o.). L. edodes extract at a dose of 200 mg/kg was administered to the paracetamol treated mice for seven days. The effects of L. edodes extract on serum transaminases (SGOT, SGPT), alkaline phosphatase (ALP) and bilirubin were measured in the paracetamol-induced hepatotoxic mice. L. edodes extract produced significant (p < 0.05) hepatoprotective effects by decreasing the activity of serum enzymes and bilirubin.

    CONCLUSIONS: From these results, it was suggested that L. edodes extract could perhaps protect liver cells from paracetamol-induced liver damage by its antioxidative effect on hepatocytes, hence diminishing or eliminating the harmful effects of toxic metabolites of paracetamol.

    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  9. Zyoud SH, Awang R, Sulaiman SA, Al-Jabi SW
    Basic Clin Pharmacol Toxicol, 2010 Nov;107(5):887-92.
    PMID: 20456332 DOI: 10.1111/j.1742-7843.2010.00594.x
    Identifying indices of poor prognosis at first presentation after acetaminophen poisoning is the key to both improving clinical care and determining targets for intervention. This study intended to document the prevalence, clinical characteristics and predictors of vomiting and to investigate the relationship between episodes of vomiting at first hospital presentation and outcome in acetaminophen poisoning. This retrospective cohort study included patients who attended the emergency department and were admitted within 24 hr of acetaminophen ingestion. The study was conducted over a period of 5 years from 1 January 2004 to 31 December 2008. Parametric and non-parametric tests were used to test differences between groups depending on the normality of the data. SPSS 15 was used for data analysis. Data from 291 patients were included. Vomiting was present in 65.3% of patients with acetaminophen poisoning at the time of first presentation. Multiple logistic regression showed that significant risk factors for vomiting were present among patients who reported an ingested dose of acetaminophen ≥10 g (p < 0.001) and a latency time of more than 8 hr (p = 0.030). Overall, an increasing trend in prothrombin time (p = 0.03), serum bilirubin (p < 0.001), serum creatinine (p = 0.005), serum potassium (p < 0.001), length of hospital stay (p < 0.001) and the prevalence of patients who had a serum acetaminophen level above a 'possible toxicity' treatment line (p = 0.001) were associated with an increased number of episodes of vomiting. In conclusion, vomiting was common among patients with acetaminophen poisoning. This study suggests that an increase in episodes of vomiting at first presentation appears to be an important risk marker of subsequent nephrotoxicity and hepatotoxicity.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  10. Ng LC, Lee YY, Lee CK, Wong SM
    Int J Dermatol, 2013 Jan;52(1):102-5.
    PMID: 23278617 DOI: 10.1111/j.1365-4632.2011.05436.x
    BACKGROUND: Methotrexate (MTX) is a common and efficacious systemic agent used for the treatment of moderate to severe psoriasis. Nevertheless, its use is associated with the risk of hepatotoxicity. This study was performed to study the association of MTX dose with regards to hepatotoxicity as evidenced by deranged transaminases.
    METHODS: This was a retrospective review of patients with psoriasis on MTX from 2000 to 2009 at the outpatient dermatology clinic, University Malaya Medical Centre (UMMC). We analyzed patients' demography, serial laboratory investigations, liver ultrasounds, and liver biopsies of patients on MTX.
    RESULTS: Sixty-six of 710 (9.30%) patients with psoriasis were prescribed MTX throughout the 10-year period. Among them 57.6% developed deranged transaminases, with six requiring MTX withdrawal due to hepatotoxicity. The mean cumulative dose of MTX at the detection of liver enzyme derangement was 552.3 ± 596.1 mg.
    CONCLUSION: A high proportion of patients on MTX had deranged transaminases. However, the number of serious events was low. We concluded from this study that the use of MTX is relatively safe in patients with moderate to severe psoriasis.

    Study site: outpatient dermatology clinic, University Malaya Medical Centre (UMMC
    Matched MeSH terms: Drug-Induced Liver Injury/etiology*
  11. Ansar S, Iqbal M
    Hum Exp Toxicol, 2016 Dec;35(12):1305-1311.
    PMID: 26825963
    The present study was undertaken to evaluate the effect of diallylsulphide (DAS) against mercuric chloride (HgCl2)-induced oxidative stress in rat livers. Rats were randomly divided into four groups of six rats each and exposed to HgCl2 (50 mg/kg/body weight (b.w.)) intraperitoneally and/or DAS (200 mg/kg/b.w.) by gavage. HgCl2 administration enhanced alanine aminotransferase (AST) and aspartate aminotransferase (ALT) levels (p < 0.05) with reduction in the levels of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). However, treatment with DAS markedly attenuated HgCl2-induced biochemical alterations in liver and serum transaminases (AST and ALT; p < 0.05). Further, biochemical results were confirmed by histopathological changes as compared to HgCl2-intoxicated rats. Histopathology of liver also showed that administration of DAS significantly reduced the damage generated by HgCl2 The present study suggests that DAS shows antioxidant activity and plays a protective role against mercury-induced oxidative damage in the rat livers.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  12. Boo YL, Liam CCK, Toh SG, Lim SM
    Hong Kong Med J, 2019 04;25(2):162-163.
    PMID: 30971509 DOI: 10.12809/hkmj187420
    Matched MeSH terms: Drug-Induced Liver Injury/etiology*
  13. Zakaria ZA, Kamisan FH, Omar MH, Mahmood ND, Othman F, Abdul Hamid SS, et al.
    BMC Complement Altern Med, 2017 May 18;17(1):271.
    PMID: 28521788 DOI: 10.1186/s12906-017-1781-5
    BACKGROUND: The present study investigated the potential of methanolic extract of Dicranopteris linearis (MEDL) leaves to attenuate liver intoxication induced by acetaminophen (APAP) in rats.

    METHODS: A group of mice (n = 5) treated orally with a single dose (5000 mg/kg) of MEDL was first subjected to the acute toxicity study using the OECD 420 model. In the hepatoprotective study, six groups of rats (n = 6) were used and each received as follows: Group 1 (normal control; pretreated with 10% DMSO (extract's vehicle) followed by treatment with 10% DMSO (hepatotoxin's vehicle) (10% DMSO +10% DMSO)), Group 2 (hepatotoxic control; 10% DMSO +3 g/kg APAP (hepatotoxin)), Group 3 (positive control; 200 mg/kg silymarin +3 g/kg APAP), Group 4 (50 mg/kg MEDL +3 g/kg APAP), Group 5 (250 mg/kg MEDL +3 g/kg APAP) or Group 6 (500 mg/kg MEDL +3 g/kg APAP). The test solutions pre-treatment were made orally once daily for 7 consecutive days, and 1 h after the last test solutions administration (on Day 7th), the rats were treated with vehicle or APAP. Blood were collected from those treated rats for biochemical analyses, which were then euthanized to collect their liver for endogenous antioxidant enzymes determination and histopathological examination. The extract was also subjected to in vitro anti-inflammatory investigation and, HPLC and GCMS analyses.

    RESULTS: Pre-treatment of rats (Group 2) with 10% DMSO failed to attenuate the toxic effect of APAP on the liver as seen under the microscopic examination. This observation was supported by the significant (p liver enzymes of alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP), and significant (p liver cells architecture with increase in dose of the extract. MEDL also demonstrated a low to none inhibitory activity against the respective LOX- and NO-mediated inflammatory activity. The HPLC and GCMS analyses of MEDL demonstrated the presence of several non-volatile (such as rutin, gallic acid etc.) and volatile (such as methyl palmitate, shikimic acid etc.) bioactive compounds.

    CONCLUSION: MEDL exerts hepatoprotective activity against APAP-induced intoxication possibly via its ability to partly activate the endogenous antioxidant system and presence of various volatile and non-volatile bioactive compounds that might act synergistically to enhance the hepatoprotective effect.

    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  14. Rengarajan T, Rajendran P, Nandakumar N, Lokeshkumar B, Balasubramanian MP
    J Environ Pathol Toxicol Oncol, 2015;34(4):287-98.
    PMID: 26756422
    The aim of the study was to evaluate the protective activity of D-Pinitol against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. The animals were divided into six groups, with each group consisting of six animals. Group I animals served as normal controls and received olive oil vehicle (1.0 ml/kg body weight intraperitoneally). Group II rats served as CCl4 controls, which received 30% CCl4 suspended in olive oil (3.0 ml/kg body weight intraperitoneally) twice a week for 4 weeks. Group III rats were treated with 30% CCl4 suspended in olive oil (3.0 ml/kg body weight intraperitoneally) twice a week for 4 weeks, followed by D-Pinitol (100 mg/kg body weight) given for 28 days intragastrically. Group IV rats received D-Pinitol alone at a concentration of 100 mg/kg body weight for 28 days intragastrically. At the end of the experimental period, serum marker enzymes and lipid peroxidation (LPO) levels were significantly increased in group II animals. On the other hand, D-Pinitol treatment significantly decreased marker enzymes and LPO levels and increased the antioxidant level. CYP expression was also investigated. Therefore, the present study revealed that D-Pinitol acts as a protective agent by decreasing metabolic activation of xenobiotics through its antioxidant nature.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  15. Shah MD, D'Souza UJA, Iqbal M
    Environ Health Prev Med, 2017 Sep 11;22(1):66.
    PMID: 29165163 DOI: 10.1186/s12199-017-0673-0
    BACKGROUND: This study aims to assess the hepatoprotective potential of Commelina nudiflora against CCl4-induced hepatic injury in rats.

    METHOD: Antioxidant activities were determined. Phytochemical analysis was performed by gas chromatography mass spectrometry (GCMS). In the in vivo study, Sprague Dawley rats were pretreated with C. nudiflora (150, 300, and 450 mg kg body weight (b.wt.)) once daily for 14 days followed by two doses of CCl4 (1 ml/kg b.wt.). After 2 weeks, the rats were sacrificed and hepatoprotective analysis was performed.

    RESULTS: In vitro studies have shown that the extract possessed strong antioxidant activity and has ability to scavenge 2,2-diphenyl-2-picrylhydrazyl-free radicals effectively. GCMS analysis of the C. nudiflora extract revealed the presence of various bioactive compounds. Administration of C. nudiflora significantly reduced the impact of CCl4 toxicity on serum markers of liver damage, serum aspartate transaminase (AST), and alanine transaminase (ALT). C. nudiflora also increased antioxidant levels of hepatic glutathione (GSH) and antioxidant enzymes and ameliorated the elevated hepatic formation of malondialdehyde (MDA) induced by CCl4 in rats. Histopathological examination indicated that C. nudiflora protect the liver from the toxic effect of CCl4 and healed lesions such as necrosis, fatty degeneration, and hepatocyte injury as irregular lamellar organization and dilations in the endoplasmic reticulum. The immunohistochemical studies revealed that pretreatment of C. nudiflora decreased the formation of 4-hydroxy-2-nonenal (HNE)-modified protein adducts and 8-hydroxy-2'-deoxyguanosine (8-OHdG). Furthermore, overexpression of the proinflammatory cytokines TNF-α, IL-6, and prostaglandin E2 is also reduced.

    CONCLUSION: These findings exhibited the potential prospect of C. nudiflora as functional ingredients to prevent ROS-related liver damage.

    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  16. Somchit N, Norshahida AR, Hasiah AH, Zuraini A, Sulaiman MR, Noordin MM
    Hum Exp Toxicol, 2004 Nov;23(11):519-25.
    PMID: 15625777
    Itraconazole and fluconazole are oral antifungal drugs, which have a wide spectrum antifungal activity and better efficacy than the older drugs. However, both drugs have been associated with hepatotoxicity in susceptible patients. The mechanism of antifungal drug-induced hepatotoxicity is largely unknown. Therefore, the aim of this present study was to investigate and compare the hepatotoxicity induced by these drugs in vivo. Rats were treated intraperitoneally with itraconazole or fluconazole either single (0, 10, 100 and 200 mg/kg) or subchronic (0, 10, 50 and 100 mg/kg per day for 14 days) doses. Plasma and liver samples were taken at the end of the study. A statistically significant and dose dependent increase of plasma alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities were detected in the subchronic itraconazole-treated group. In addition, dose-dependent hepatocellular necrosis, degeneration of periacinar and mizonal hepatocytes, bile duct hyperplasia and biliary cirrhosis and giant cell granuloma were observed histologically in the same group. Interestingly, fluconazole treated rats had no significant increase in transaminases for both single and subchronic groups. In the subchronic fluconazole treated rats, only mild degenerative changes of centrilobular hepatocytes were observed. These results demonstrated that itraconazole was a more potent hepatotoxicant than fluconazole in vivo in rats.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  17. Ansar S, Iqbal M
    Hum Exp Toxicol, 2016 Mar;35(3):259-66.
    PMID: 25904316 DOI: 10.1177/0960327115583362
    Garlic contains diallylsulfide (DAS) and other structurally related compounds that are widely believed to be active agents in preventing cancer. This study shows the effect of DAS (a phenolic antioxidant used in foods, cosmetics, and pharmaceutical products) on ferric nitrilotriacetate (Fe-NTA)-induced hepatotoxicity in rats. Male albino rats of Wistar strain weighing 125-150 g were given a single dose of Fe-NTA (9 mg kg(-1) body weight, intraperitoneally) after 1 week of treatment with 100 and 200 mg kg(-1) DAS in corn oil respectively administered through the gavage. Fe-NTA administration led to 2.5-fold increase in the values of both alanine transaminase and aspartate aminotransferase, respectively, and 3.2-fold increase in the activity of lactate dehydrogenase, microsomal lipid peroxidation to approximately 2.0-fold compared to saline-treated control. The activities of glutathione (GSH) and other antioxidant enzymes decreased to a range of 2.2-2.5-fold. These changes were reversed significantly (p < 0.001) in animals receiving a pretreatment of DAS. DAS protected against hepatic lipid peroxidation, hydrogen peroxide generation, preserved GSH levels, and GSH metabolizing enzymes to 60-80% as compared to Fe-NTA alone-treated group. Present data suggest that DAS can ameliorate the toxic effects of Fe-NTA and suppress oxidant-induced tissue injury and hepatotoxicity in rats.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  18. Mohamad Shalan NAA, Mustapha NM, Mohamed S
    Regul Toxicol Pharmacol, 2017 Feb;83:46-53.
    PMID: 27871867 DOI: 10.1016/j.yrtph.2016.11.022
    Noni (Morinda citrifolia) leaf and fruit are used as food and medicine. This report compares the chronic toxicity of Noni fruit and edible leaf water extracts (two doses each) in female mice. The 6 months study showed the fruit extract produced chronic toxicity effects at the high dose of 2 mg/ml drinking water, evidenced through deteriorated liver histology (hepatocyte necrosis), reduced liver length, increased liver injury marker AST (aspartate aminotransferase) and albumin reduction, injury symptoms (hypoactivity, excessive grooming, sunken eyes and hunched posture) and 40% mortality within 3 months. This hepatotoxicity results support the six liver injury reports in humans which were linked to chronic noni fruit juice consumption. Both doses of the leaf extracts demonstrated no observable toxicity. The hepatotoxicity effects of the M. citrifolia fruit extract in this study is unknown and may probably be due to the anthraquinones in the seeds and skin, which had potent quinone reductase inducer activity that reportedly was 40 times more effective than l-sulforaphane. This report will add to current data on the chronic toxicity cases of Morinda citrifolia fruit. No report on the chronic toxicity of Morinda citrifolia fruit in animal model is available for comparison.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology*
  19. Wu X, Zhang S, Lai J, Lu H, Sun Y, Guan W
    Exp Clin Transplant, 2020 12;18(7):823-831.
    PMID: 33349209 DOI: 10.6002/ect.2020.0108
    OBJECTIVES: Liver fibrosis is inevitable in the healing process of liver injury. Liver fibrosis will develop into liver cirrhosis unless the damaging factors are removed. This study investigated the potential therapy of Bama pig adipose-derived mesenchymal stem cells in a carbon tetrachloride-induced liver fibrosis Institute of Cancer Research strain mice model.

    MATERIALS AND METHODS: Adipose-derived mesenchymal stem cells were injected intravenously into the tails of mice of the Institute of Cancer Research strain that had been treated with carbon tetrachloride for 4 weeks. Survival rate, migration, and proliferation of adipose-derived mesenchymal stem cells in the liver were observed by histochemistry, fluorescent labeling, and serological detection.

    RESULTS: At 1, 2, and 3 weeks after adipose-derived mesenchymal stem cell injection, liver fibrosis was significantly ameliorated. The injected adipose-derived mesenchymal stem cells had hepatic differentiation potential in vivo, and the survival rate of adipose-derived mesenchymal stem cells declined over time.

    CONCLUSIONS: The findings in this study confirmed that adipose-derived mesenchymal stem cells derived from the Bama pig can be used in the treatment of liver fibrosis, and the grafted adipose-derived mesenchy-mal stem cells can migrate, survive, and differentiate into hepatic cells in vivo.

    Matched MeSH terms: Drug-Induced Liver Injury/etiology
  20. Abd Rashid N, Abd Halim SAS, Teoh SL, Budin SB, Hussan F, Adib Ridzuan NR, et al.
    Biomed Pharmacother, 2021 Dec;144:112328.
    PMID: 34653753 DOI: 10.1016/j.biopha.2021.112328
    Cisplatin is a potent platinum-based anticancer drug approved by the Food Drug Administration (FDA) in 1978. Despite its advantages against solid tumors, cisplatin confers toxicity to various tissues that limit its clinical uses. In cisplatin-induced hepatotoxicity, few mechanisms have been identified, which started as excess generation of reactive oxygen species that leads to oxidative stress, inflammation, DNA damage and apoptosis in the liver. Various natural products, plant extracts and oil rich in flavonoids, terpenoids, polyphenols, and phenolic acids were able to minimize oxidative stress by restoring the level of antioxidant enzymes and acting as an anti-inflammatory agent. Likewise, treatment with honey and royal jelly was demonstrated to decrease serum transaminases and scavenge free radicals in the liver after cisplatin administration. Medicinal properties of these natural products have a promising potential as a complementary therapy to counteract cisplatin-induced hepatotoxicity. This review concentrated on the protective role of several natural products, which has been proven in the laboratory findings to combat cisplatin-induced hepatotoxicity.
    Matched MeSH terms: Drug-Induced Liver Injury/etiology
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