A Review of the Role of Curcumin in Metal Induced Toxicity
Abstract
:1. Introduction
2. Curcumin as a Bioactive Compound in Turmeric Plant
3. Chemical Properties of Curcumin
4. Bioavailability of Curcumin
5. General Perspective of Curcumin in the Protection of Metal Toxicity
6. Curcumin on Aluminum-Induced Toxicity
7. Curcumin on Arsenic-Induced Toxicity
Dose/Concentration | Name of Animal Model/Cell Lines | Route of Exposure | Duration of Exposure/Treatment | Results | Source |
---|---|---|---|---|---|
Clinical Trial | |||||
CUR + piperine (20:1) 2 × 500 mg/day | Chronically arsenic-exposed males or females | Orally | 6 months | ↓DNA damage, ↓ROS generation, ↓CAT, SOD enzymes, | [111] |
CUR + piperine (100:1) 500 mg twice/day | Chronically arsenic-exposed males or females | Orally | 6 months | ↑expression of protein, mRNA of DNA-PK, DNA ligase IV, XRCC4, ↑BER and NHEJ repair pathways, ↓DNA-damaging effect in lymphocytes | [112] |
In Vivo | |||||
5 mg/kg b.w. NaAsO2 + 15 mg/kg b.w. CUR | Male Wistar rats | NaAsO2-orally/CUR-orally | 30 days (co-administration) | ↓transaminases, phosphatases, glucose, urea, creatinine, bilirubin, TL, cholesterol, TG, plasma and brain ache, the levels of TP and Alb | [113] |
5 or 300 ppm NaAsO2 + 0.5 mg/kg b.w. nano-CUR | Male Swiss albino mice | NaAsO2-drinking water/CUR-orally | NaAsO2-7 days/CUR-14 days(post-treatment) | ↓histopathological alterations, ↓accumulation of acidic vesicles, ↓apoptotic cells in the thymus and spleen, ↓autophagy, ↓redox imbalance in immune cells | [115] |
In Vitro | |||||
10 μM NaAsO2 + 0, 1, 2.5, 5, 10, 25, 50 or 100 μM CUR | PC12 cells | Cell line | 24 h | ↑membrane integrity, ↓DNA damage, apoptosis rate, ↑protein expressions, ↑cell viability, ↑cytoprotective effect, ↓oxidative stress | [114] |
8. Curcumin on Cadmium-Induced Toxicity
9. Curcumin on Copper-Induced Toxicity
10. Curcumin on Iron-Induced Toxicity
11. Curcumin on Lead-Induced Toxicity
Dose/Concentration | Name of Animal Model/Cell Lines | Route of Exposure | Duration of Exposure/Treatment | Results | Source |
---|---|---|---|---|---|
In Vivo | |||||
50 mg/kg Pb(C2H3O2)2 + 100 mg/kg CUR 50 mg/kg Pb(C2H3O2)2 + 200 mg/kg CUR | Male Sprague–Dawley rats | Pb(C2H3O2)2, CUR- orogastric tube | Pb(C2H3O2)2-4 weeks/CUR-4 weeks (post-treatment) | ↓Pb concentration, ↓oxidative stress, ↓cerebellar damage in cerebellum, ↑motor coordination | [155] |
50 mg/kg Pb(C2H3O2)2 + 200 mg/kg CUR | Male Wistar rats | Pb(C2H3O2)2 -IP/CUR-orally | 7 days (co-administration) | ↓apoptosis, ↓oxidative stress, ↓inflammation, ↓liver injury, ↑AKT/GSK-3β signaling pathway | [157] |
20 mg/kg OD Pb(C2H3O2)2 + 30 mg/kg BD CUR | Male and female Wistar rats | Pb(C2H3O2)2, CUR- IP | 5 days (co-administration) | ↓damage neurons, ↓protein oxidation, lipid peroxidation, ↑GSH | [158] |
1 mg/L Pb + 15 g/kg CUR | Cyprinus carpio | Pb-aquarium water/CUR-orally | 8 weeks (co-administration) | ↓mRNA, expression of NF-kB p65, ↓AST, ALT, LDH, ↑protease activity, ↑SOD, GPx, GSH, G-Rd, GST, Nrf2, ↑lysozyme activity, C3, IgM, ↑intestinal microbial abundance, ↑growth parameters, ↑RBC, Hct, Hb, serum protein, albumin, ↑enzymatic activities, ↑IL-10, ↓MDA | [154] |
In Vitro | |||||
10 μM Pb(C2H3O2)2 + 50, 100, or 150 μM CUR | Rat pups’ hippocampi | 3 h | ↓free radicals, ↑cell viability | [158] |
12. Curcumin on Zinc-Induced Toxicity
Dose/Concentration | Name of Animal Model/Cell Lines | Route of Exposure | Duration of Exposure/Treatment | Results | Source |
---|---|---|---|---|---|
In Vivo | |||||
5.6 mg/kg b.w. ZnONP + 200 mg/kg CUR | Male albino rats | ZnONP-IP/CUR-oral gavage | ZnONP-28 days (started on day 7, three times per week)/CUR-28 days (pre-treatment) | ↑cerebellum structure, ↓oxidative stress markers, ↑inflammatory response, ↓COX-2, P53 | [52] |
50 mg/kg ZnONP + 200 mg/kg CUR | Male Wistar rats | ZnONP, CUR-orally | ZnONP-14 days (started on day 7)/CUR-14 days (pre-treatment) | ↑body, kidney weight, ↓MDA in the renal tissue, ↑SOD, GPx, ↓histological changes, ↓apoptotic index | [162] |
50 mg/kg nano-ZnO + 200 mg/kg CUR | Male Wistar rats | ZnO-gavage method/ CUR- oral gavage | ZnO-21 days (started on day 7)/CUR-21 days (pre-treatment)2 | ↓lipid peroxidation, ↑SOD, GPx ↓ALT, AST, ALP, ↓histology changes, ↓apoptotic index of hepatocytes | [163] |
13. Curcumin on Mercury-Induced Toxicity
14. Curcumin on Selenium-Induced Toxicity
15. Curcumin on Chromium-Induced Toxicity
16. Conclusions and Future Outlook
Author Contributions
Funding
Data Availability Statement
Acknowledgments
Conflicts of Interest
References
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Metal | HBGV | Value | Source |
---|---|---|---|
Aluminum | TWI | 2000 μg/kg b.w. | [12] |
TDI | 10,000 μg/kg b.w. | [13] | |
Arsenic | TWI | 15 μg/kg b.w. | [14] |
Cadmium | TWI | 2.5 µg/kg b.w. | [15] |
Chromium | TDI | 300 μg/kg b.w. | [16] |
Cobalt | TDI | 1.4 μg/kg b.w. | [17] |
Copper | UL | 10,000 μg/kg b.w. | [18] |
Iron | TDI | 800 µg/kg b.w. | [19] |
Lead | TWI | 25 µg/kg b.w. | [20] |
TDI | 600 µg/kg b.w. | ||
Manganese | TDI | 60 µg/kg b.w. | [21] |
Mercury | TWI | 4 µg/kg b.w. | [22] |
Nickel | TDI | 12 μg/kg b.w. | [23] |
Selenium | UL | 400 μg/kg b.w. | [24] |
Zinc | UL | 40,000 μg/day | [18] |
Dose/Concentration | Name of Animal Model/Cell Lines | Route of Exposure | Duration of Exposure/Treatment | Results | Source |
---|---|---|---|---|---|
100 mg/kg b.w. Al + 50 mg/kg b.w. CUR | Sprague–Dawley rats | Al-drinking water/CUR-IP | Al-8 weeks/CUR-2 months (co-administration) | ↓TNF-α, ↓NF-kB p65, ↓NO activity | [100] |
50 mg/kg/day Al + 30 mg/mL/kg b.w. CUR | Male Wistar rats | Al-drinking water/CUR-orally | 6 months (co-administration) | ↓lipid peroxidation in the brain, ↓SOD, GPx, GST and Na+, K+, ATPase | [107] |
100 mg/kg Al + 30 or 60 mg/kg CUR | Male Wistar rats | Al-drinking water/CUR-orally | 42 days(co-administration) | ↓IAL, first and second RL to reach the platform in the pre-trained rats, ↑retention performance of the spatial navigation task; ↓MDA, nitrite levels, ↑reduced GSH, ↓GST, SOD, and catalase activity, ↓AChE activity, ↓Al in hippocampus | [104] |
Synthesized [Al(CUR) (EtOH)2](NO3)2) complex | Binding of CUR complex to calf thymus-DNA | ↓affinity of Al to interact with DNA | [103] | ||
Synthesized Al (III)–CUR complexes | NMR, mass spectroscopy, ultraviolet, the generalized 2D UV–UV correlation spectroscopy, the density functional theory | ↓affinity of Al to interact with amyloid beta (Aβ) peptide, ↓ toxicity effect of Al on peptides, ↓ oxidative stress | [102] |
Dose/Concentration | Name of Animal Model/Cell Lines | Route of Exposure | Duration of Exposure/Treatment | Results | Source |
---|---|---|---|---|---|
In Vivo | |||||
0.8 mg/L water Cd + basal diet with 0.5% TP | Juvenile African catfish | Cd-aquarium water/TP-orally | 30 days (co-administration) | ↑growth rate, ↑HSI, ↓damage to the hepatic architecture, the testis architecture, ↑reproduction hormone level, lysozyme activity, immunoglobulin levels, protein content, ATP content, ↓disturbed enzyme activities, ↓nephrotoxicity, ↓oxidative stress, ↓apoptotic events, ↓Cd accumulation in muscles, the liver | [124] |
40 mg/L CdCl2 + 50 mg/kg b.w. CUR | Male albino rats | Cd-drinking water/CUR-gastric tube | 6 weeks (co-administration) | ↓TNF-α, IL-6, ↓lipid peroxidation, ↑CAT, SOD, GSH, TAC, ↓oxidative stress, ↓loss of antioxidant enzymes | [122] |
200 mg/kg b.w. C4H6CdO4 + 250 mg/kg b.w. CUR | Adult male rats | Cd-drinking water/CUR-orally | 7 days (co-administration) | ↓level of urea, creatinine in the serum, ↑antioxidant levels | [125] |
1 mg/kg b.w. Cd + 100 mg/kg b.w. CUR | Male Wistar albino rats | Cd-subcutaneously/CUR-intragastric intubation | 4 weeks (co-administration) | ↓testicular damage, ↓reactivity and the number of germ cell, Leydig cell apoptosis, ↓TUNEL positive cells of testis | [126] |
1 mg/kg/day or 100 mg/kg/day CdCl2 + 1 mg/kg/day or 100 mg/kg/day CUR | Male Spraque–Dawley rats | CdCl2-IP/CUR-orally | 3 days (co-administration) | ↓TBARS levels, ↑GSH, CAT, GPx, SOD, ↓histopathological changes, ↓lipid peroxidation, ↓oxidative stress in testis tissue, ↑antioxidant enzymes | [127] |
7 mg/kg b.w. CdCl2 + 50 mg/kg b.w. CUR | Male CD mice | CdCl2- subcutaneously/CUR-orally | CdCl2-ones/CUR-3 days (pre-treatment) | ↑GSH, GPx, ↑antioxidant status, ↔Cd level in tissues, ↓lipid peroxidation | [121] |
0.025 mmol/kg b.w. (rats), 0.03 mmol/kg b.w. (mice) CdCl2 + 50 mg/kg b.w. CUR | Male Wistar rats, male CD mice | CdCl2- subcutaneously/CUR-orally | CdCl2-ones/CUR-3 days (pre-treatment) | ↓lipid peroxidation | [128] |
5 mg/kg b.w. CdCl2 + 200 or 400 mg/kg b.w. CUR | Adult male Wistar rats | CdCl2- oral gavage/CUR-oral gavage | 27 days (co-administration) | ↓MDA, ↑GSH, ↓nephrotoxicity | [129] |
5 mg/kg b.w. CdCl2 + 200 or 400 mg/kg b.w. CUR | Adult male ICR mice | Cd-drinking water/CUR-intragastric | 8 weeks (co-administration) | ↓systolic, diastolic, and mean arterial blood pressure levels, ↑Phe, Ach, and SNP, ↓hypertension, ↓impairment of vascular responsiveness to vasoactive agents, ↓lipid peroxidation, ↓protein oxidation, ↑GSH, ↑redox status of the blood cells, ↓oxidants, ↑endogenous antioxidant formation, ↓oxidative stress, ↓Cd accumulation in the blood, organs | [130] |
In Vitro | |||||
100 mM CdSO4 + 10, 30, 20, 40 or 50 μM CUR | Bronchial epithelial cell line Calu-3 | 24 h | ↓IL-6, IL-8 mRNA transcript levels, ↓Erk1/2 activation | ||
0.025, 0.05, 0.1 mM CdCl2 + 0.025, 0.05, 0.1 mM CUR | Rat brain homogenate | Lipid peroxidation assay | ↓lipid peroxidation | [131] |
Dose/Concentration | Name of Animal Model/Cell Lines | Route of Exposure | Duration of Exposure/Treatment | Results | Source |
---|---|---|---|---|---|
In Vivo | |||||
100 mg/kg CuSO4 + 80 mg/kg CUR; 100 mg/kg CuSO4 + 80 mg/kg nano-CUR | Male Wistar rats | Cu-orally/CUR-orally | 7 days (co-administration) | ↓cerebral oxidative stress, ↓cerebral inflammation in stress, ↓apoptosis, ↑AKT/GSK-3β signaling pathway, ↑BDNF | [82] |
250 mg/kg CuONP + 200 mg/kg b.w. CUR | Rats | CuONP-oral gavage/CUR- orally | 3 months (co-administration) | ↑body weight gain, ↓serum creatinine, BUN levels, ↓KIM-1 in urine, kidney, ↓oxidative stress, ↓NO level, ↓mRNA expression of IL1-β, TNF-α, NF-ĸB ↑Nrf2, HO-1, γ-GCS gene expression in the kidney, ↓renal damage, ↓morphological tubular, glomerular alteration, ↓caspase-3 | [138] |
1 mM Cu + 0.2 or 0.5 mg/kg CUR | Drosophila melanogaster wild-type (Harwich strain) flies | Cu, CUR-medium | 7 days (co-administration) | ↓oxidative stress, ↓nitrite level, ↓AChE activity, ↓dopamine levels | [140] |
4 mg/kg CuSO4 + 80 mg/kg CUR | Albino rats | CuSO4, CUR- orally by stomach tube | 30 days (co-administration) CuSO4-15 days/CUR-15 days (post-treatment) | ↓hepatic marker enzymes, ↑hepatic, renal antioxidants, MDA, ↓renal tissue damage, ↑antioxidant enzymes, ↓ROS | [141] |
Other | |||||
Cu2+, Zn2+, Fe2+ + CUR | Spectrophotometry | Binding more readily Fe and Cu than Zn, ↓Aβ toxicity, ↓NF-κB | [142] |
Dose/Concentration | Name of Animal Model/Cell Lines | Route of Exposure | Duration of Exposure/Treatment | Results | Source |
---|---|---|---|---|---|
In Vivo | |||||
30 mg FeSO4 in 1 mL saline ⁄ kg b.w. + basal diet with 0.2 g% CUR | Male Wistar rats | FeSO4-IP/CUR- oral gavage | FeSO4-ones/CUR-8 weeks (pre-treatment) | ↓LDL oxidation, ↓ALT, AST, LDH, ↓liver lipid peroxide level, ↓severity of hepatotoxicity | [147] |
In Vitro | |||||
250 µM or 500 µM Fe-NTA + 20 μM or 50 μM CUR | Huh-7, T51B, RL-34 cells | 24, 48, 72, 96, 120 h | ↑tumor-promoting effect, ↑Fe2+ chelating, ↔Fe uptake | [94] | |
200 µM FAC + 50 µM CUR | T51B cell line | 5 or 10 days | ↑Fe chelating, ↔Fe uptake/bioavailability, ↓ROS, ↓signaling to cellular stress pathways, | [148] | |
50 μmol/L FAC or 30 μmol/L FeSO4 + 20 μM CUR | Mouse MIN6 pancreatic β-cell line | 24 h | ↓cell damage, ↑stress protection, ↓cell mortality, ↓Fe accumulation, ↓MDA, ↑GSH | [146] |
Dose/Concentration | Name of Animal Model/Cell Lines | Route of Exposure | Duration of Exposure/Treatment | Results | Source |
---|---|---|---|---|---|
In Vivo | |||||
12 µmol/kg b.w. HgCl2 + 80 mg/kg b.w. CUR | Male Wistar rats | HgCl2-IP/CUR-orally | HgCl2-ones(pre/post-treated groups)/CUR-3 days(post-treatment, pre-treatment) | ↓oxidative stress, ↓lipid peroxidation, ↑GSH, SOD GPx, CAT in the liver, kidney, brain, ↓serum biochemical changes, ↓Hg in tissues | [168] |
5 mg/kg HgCl2 + 50 mg/kg b.w. CUR | Kunming male mice | HgCl2, CUR-IP | HgCl2-ones/CUR-24 h (pre-treatment) | ↓autophagic cell death, ↓Na overload, ↓Ca leak, ↑Nrf2 signaling pathway, ↑antioxidant defenses | [169] |
10 ppm HgCl2 + 150 or 300 ppm CUR | Pregnant Swiss-Webster strain mice | HgCl2, CUR-oral gavage | 15 days (co-administration) | ↓biochemical, behavioral disorders, ↑cognitive, anxiety behaviors | [170] |
Dose/Concentration | Name of Animal Model/Cell Lines | Route of Exposure | Duration of Exposure/Treatment | Results | Source |
---|---|---|---|---|---|
In Vivo | |||||
15 µM/kg b.w. Se + 75 mg/kg b.w. CUR | Wistar rats | Se-IP/CUR-orally | Se-ones(co/pre/post-treated groups)/CUR-ones (co-administration, post-treatment, pre-treatment) | ↓liver cells damage, ↓architecture changes of glomeruli and tubules, ↓iNOS | [175] |
15 µM/kg b.w. Se + 75 mg/kg b.w. CUR | Wistar rat pups | Se-IP/CUR-orally | Se-ones(co/pre/post-treated groups)/CUR-ones (co-administration, post-treatment, pre-treatment) | ↓LPO, ↓SOD, GST, GPx, CAT, ↓GSH, vitamin C, vitamin E | [177] |
In Vitro | |||||
100 μM Na2SeO3 + 100 μM or 200 μM CUR | Wistar Rat pups | Isolated lenses incubation in DMEM | 62 h | ↓oxidative stress, ↓cataract formation | [176] |
Dose/Concentration | Name of Animal Model/Cell Lines | Route of Exposure | Duration of Exposure/Treatment | Results | Source |
---|---|---|---|---|---|
In Vivo | |||||
0.4 mg/kg b.w. OD K2Cr2O7 + 20 mg/kg b.w. CUR | Male albino rats of Sprague–Dawley strain Rattus norvegicus | K2Cr2O7,CUR-IP | K2Cr2O7-26 days/CUR-26 days(every alternate day) (co-administration) | ↓testicular histology damage, ↑sperm count, ↑testosterone level, ↑accessory sex organs weight, ↓lipid peroxidation, ↑SOD, CAT | [180] |
015 mg/kg b.w. K2Cr2O7 + 100, 200 or 400 mg/kg b.w. CUR | Male Wistar rats | K2Cr2O7- subcutaneously/CUR- gavage | K2Cr2O7-ones(co/pre/post-treated groups)/ /CUR- 10 days before and 2 days after K2Cr2O7 injection (co-administration, post-treatment, pre-treatment) | ↓renal dysfunction, ↓histological damage, ↓oxidant stress, ↑antioxidant enzymes, ↔Cr in renal homogenates, in mitochondria (pre-treated), ↑mitochondrial oxygen consumption, ↑activity of mitochondrial complexes I, II, II–III, V, ↑mitochondrial ATP content, ↑mitochondrial Ca2+ transport, mitochondrial membrane potential, ↔Cr concentration, ↑nuclear translocation of Nrf2, ↑GST | [181] |
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Smirnova, E.; Moniruzzaman, M.; Chin, S.; Sureshbabu, A.; Karthikeyan, A.; Do, K.; Min, T. A Review of the Role of Curcumin in Metal Induced Toxicity. Antioxidants 2023, 12, 243. https://doi.org/10.3390/antiox12020243
Smirnova E, Moniruzzaman M, Chin S, Sureshbabu A, Karthikeyan A, Do K, Min T. A Review of the Role of Curcumin in Metal Induced Toxicity. Antioxidants. 2023; 12(2):243. https://doi.org/10.3390/antiox12020243
Chicago/Turabian StyleSmirnova, Elena, Mohammad Moniruzzaman, Sungyeon Chin, Anjana Sureshbabu, Adhimoolam Karthikeyan, Kyoungtag Do, and Taesun Min. 2023. "A Review of the Role of Curcumin in Metal Induced Toxicity" Antioxidants 12, no. 2: 243. https://doi.org/10.3390/antiox12020243
APA StyleSmirnova, E., Moniruzzaman, M., Chin, S., Sureshbabu, A., Karthikeyan, A., Do, K., & Min, T. (2023). A Review of the Role of Curcumin in Metal Induced Toxicity. Antioxidants, 12(2), 243. https://doi.org/10.3390/antiox12020243