Reviewed By
Overview
SCIENTIFIC SCORE
Possibly Effective
Based on 14 Researches
7.8
USERS' SCORE
Good
Based on 5 Reviews
8
Supplement Facts
Serving Size: 1 Spray (Approx. 0.41 ml)
Amount Per Serving
%DV
Vitamin B12(as Methylcobalamin from Saccharomyces cerevisiae)
500 mcg
20,833%
Certified Organic Food BlendOrganic Beet (root), Organic Carrot (root), Organic Spinach (leaf), Organic Broccoli (flower & stem), Organic Tomato (fruit), Organic Kale (leaf), Organic Cabbage (leaf), Organic Parsley (leaf), Organic Brussels Sprout (leaf), Organic Green Bell Pepper (fruit), Organic Cucumber (gourd), Organic Celery (stalk), Organic Garlic (bulb), Organic Ginger (root), Organic Onion (root), Organic Cauliflower (flower & stem), Organic Asparagus (flower & stem), Organic Strawberry (fruit), Organic Cherry (fruit), Organic Blackberry (fruit), Organic Blueberry (fruit), Organic Raspberry (fruit)
2 mg
+
Top Medical Research Studies
9
We explored how methylcobalamin, a form of vitamin B12, impacts liver disease, particularly in the context of cholestatic liver failure. The study utilized high-throughput screening to identify methylcobalamin as a specific inhibitor of gasdermin E (GSDME), a protein that plays a key role in pyroptotic cell death—a form of inflammatory cell death contributing to liver damage.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Read More
9
Methylcobalamin improves nerve myelination
We delved into the effects of methylcobalamin, a form of vitamin B12, on nerve myelination in rats suffering from moderate hepatic encephalopathy, a condition caused by ammonia toxicity due to liver dysfunction. In our study, we established a model of hepatic encephalopathy by administering thioacetamide to induce liver damage, subsequently leading to changes in nerve myelination in specific brain regions.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
Read More
9
We explored the intriguing question of whether vitamin B12 can provide a protective effect against liver damage caused by acetaminophen, a common painkiller known for its potential hepatotoxicity. In our study, we used male Wister rats and organized them into three groups: one receiving acetaminophen, another treated with vitamin B12, and a control group given distilled water. Each group was administered their respective treatments for a week before we evaluated their liver health.
Our findings indicate that vitamin B12 supplementation significantly improved hepatic health in the rats exposed to acetaminophen. We observed a notable reduction in liver enzyme levels, which is a key marker of liver damage. Additionally, vitamin B12 helped boost antioxidant levels in the body, compensated for a decline in tissue glutathione, and reduced harmful inflammatory markers such as TNF-α and interleukin-6.
Overall, the results of our study suggest that vitamin B12 effectively mitigates acetaminophen-induced liver toxicity by enhancing liver function and reducing inflammation. This insight opens up interesting avenues for considering vitamin B12 as a supportive treatment in managing liver health in cases of acetaminophen exposure.
Our findings indicate that vitamin B12 supplementation significantly improved hepatic health in the rats exposed to acetaminophen. We observed a notable reduction in liver enzyme levels, which is a key marker of liver damage. Additionally, vitamin B12 helped boost antioxidant levels in the body, compensated for a decline in tissue glutathione, and reduced harmful inflammatory markers such as TNF-α and interleukin-6.
Overall, the results of our study suggest that vitamin B12 effectively mitigates acetaminophen-induced liver toxicity by enhancing liver function and reducing inflammation. This insight opens up interesting avenues for considering vitamin B12 as a supportive treatment in managing liver health in cases of acetaminophen exposure.
Read More
Most Useful Reviews
9
Salvation for deficiency
1 people found this helpful
An essential vitamin for the body, especially for those with liver disease. This product provides effective support and can be a real lifesaver!
Read More
6
Improved cognitive abilities
5 people found this helpful
Good spray with a pleasant taste from a reliable manufacturer. The dose is suitable for maintenance, but if someone has a significant deficiency, such as me with liver disease, a larger dose may be necessary. Vitamin B12 accumulates in the liver, and it's essential for cognitive function. If you're experiencing poor memory or concentration, consider increasing your intake of B12.
Read More
7.5
Eliminates pain
1 people found this helpful
Vitamin B12 is crucial as it helps manage liver disease and can eliminate pain. It prevents pernicious anaemia, heart attacks, and strokes, while supporting health. The quality is excellent, made from natural ingredients, and I appreciate the packaging and the price.
Read More
Medical Researches
SCIENTIFIC SCORE
Possibly Effective
Based on 14 Researches
7.8
- All Researches
9
We explored how methylcobalamin, a form of vitamin B12, impacts liver disease, particularly in the context of cholestatic liver failure. The study utilized high-throughput screening to identify methylcobalamin as a specific inhibitor of gasdermin E (GSDME), a protein that plays a key role in pyroptotic cell death—a form of inflammatory cell death contributing to liver damage.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Read More
9
Methylcobalamin improves nerve myelination
We delved into the effects of methylcobalamin, a form of vitamin B12, on nerve myelination in rats suffering from moderate hepatic encephalopathy, a condition caused by ammonia toxicity due to liver dysfunction. In our study, we established a model of hepatic encephalopathy by administering thioacetamide to induce liver damage, subsequently leading to changes in nerve myelination in specific brain regions.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
Read More
9
We explored the intriguing question of whether vitamin B12 can provide a protective effect against liver damage caused by acetaminophen, a common painkiller known for its potential hepatotoxicity. In our study, we used male Wister rats and organized them into three groups: one receiving acetaminophen, another treated with vitamin B12, and a control group given distilled water. Each group was administered their respective treatments for a week before we evaluated their liver health.
Our findings indicate that vitamin B12 supplementation significantly improved hepatic health in the rats exposed to acetaminophen. We observed a notable reduction in liver enzyme levels, which is a key marker of liver damage. Additionally, vitamin B12 helped boost antioxidant levels in the body, compensated for a decline in tissue glutathione, and reduced harmful inflammatory markers such as TNF-α and interleukin-6.
Overall, the results of our study suggest that vitamin B12 effectively mitigates acetaminophen-induced liver toxicity by enhancing liver function and reducing inflammation. This insight opens up interesting avenues for considering vitamin B12 as a supportive treatment in managing liver health in cases of acetaminophen exposure.
Our findings indicate that vitamin B12 supplementation significantly improved hepatic health in the rats exposed to acetaminophen. We observed a notable reduction in liver enzyme levels, which is a key marker of liver damage. Additionally, vitamin B12 helped boost antioxidant levels in the body, compensated for a decline in tissue glutathione, and reduced harmful inflammatory markers such as TNF-α and interleukin-6.
Overall, the results of our study suggest that vitamin B12 effectively mitigates acetaminophen-induced liver toxicity by enhancing liver function and reducing inflammation. This insight opens up interesting avenues for considering vitamin B12 as a supportive treatment in managing liver health in cases of acetaminophen exposure.
Read More
8
We explored the potential of an engineered yeast, S. cerevisiae-pYD1-ScFv-AFB1, in addressing liver damage caused by aflatoxin B1 (AFB1), a known cancer risk factor. Using a mouse model, we treated subjects with this specialized yeast for four weeks.
The results showed that the engineered yeast significantly reduced inflammation and cellular damage in the liver, and improved antioxidant capacity. Additionally, it helped repair the intestinal barrier disrupted by AFB1. These findings suggest it may offer a new way to combat AFB1 toxicity.
The results showed that the engineered yeast significantly reduced inflammation and cellular damage in the liver, and improved antioxidant capacity. Additionally, it helped repair the intestinal barrier disrupted by AFB1. These findings suggest it may offer a new way to combat AFB1 toxicity.
Read More
8
Saccharomyces-driven protection against liver toxicity
We explored how sophorolipids, produced by Saccharomyces cerevisiae using banana peels, could guard against liver damage caused by the chemotherapy drug doxorubicin (DOX). In our study with male Wistar rats, we compared the effects of sophorolipid treatment against DOX alone.
The results showed that applying sophorolipids improved liver function and adjusted key markers related to oxidative stress and inflammation. In essence, the sophorolipids appeared to offer protection against the harmful effects of DOX on the liver.
The results showed that applying sophorolipids improved liver function and adjusted key markers related to oxidative stress and inflammation. In essence, the sophorolipids appeared to offer protection against the harmful effects of DOX on the liver.
Read More
User Reviews
USERS' SCORE
Good
Based on 5 Reviews
8
- All Reviews
- Positive Reviews
- Negative Reviews
9
Salvation for deficiency
1 people found this helpful
An essential vitamin for the body, especially for those with liver disease. This product provides effective support and can be a real lifesaver!
Read More
6
Improved cognitive abilities
5 people found this helpful
Good spray with a pleasant taste from a reliable manufacturer. The dose is suitable for maintenance, but if someone has a significant deficiency, such as me with liver disease, a larger dose may be necessary. Vitamin B12 accumulates in the liver, and it's essential for cognitive function. If you're experiencing poor memory or concentration, consider increasing your intake of B12.
Read More
7.5
Eliminates pain
1 people found this helpful
Vitamin B12 is crucial as it helps manage liver disease and can eliminate pain. It prevents pernicious anaemia, heart attacks, and strokes, while supporting health. The quality is excellent, made from natural ingredients, and I appreciate the packaging and the price.
Read More
7.5
Strengthens immune system
One of the best B12 products available! Many, regardless of their diet, are deficient in B12, which is vital for thousands of body functions daily. B12 aids in liver disease, reinforcing the immune system and repairing nerves. Be cautious with injections since they may not support necessary processes in the body.
Read More
6
Recommended for anaemia
A highly effective B12 product, beneficial for anaemia, liver disease, hypothyroidism, and high homocysteine levels. I recommend it as a working solution for such conditions.
Read More
Frequently Asked Questions
7.5
Eliminates pain
1 people found this helpful
Vitamin B12 is crucial as it helps manage liver disease and can eliminate pain. It prevents pernicious anaemia, heart attacks, and strokes, while supporting health. The quality is excellent, made from natural ingredients, and I appreciate the packaging and the price.
6
Improved cognitive abilities
5 people found this helpful
Good spray with a pleasant taste from a reliable manufacturer. The dose is suitable for maintenance, but if someone has a significant deficiency, such as me with liver disease, a larger dose may be necessary. Vitamin B12 accumulates in the liver, and it's essential for cognitive function. If you're experiencing poor memory or concentration, consider increasing your intake of B12.
6
Recommended for anaemia
A highly effective B12 product, beneficial for anaemia, liver disease, hypothyroidism, and high homocysteine levels. I recommend it as a working solution for such conditions.
9
Salvation for deficiency
1 people found this helpful
An essential vitamin for the body, especially for those with liver disease. This product provides effective support and can be a real lifesaver!
7.5
Strengthens immune system
One of the best B12 products available! Many, regardless of their diet, are deficient in B12, which is vital for thousands of body functions daily. B12 aids in liver disease, reinforcing the immune system and repairing nerves. Be cautious with injections since they may not support necessary processes in the body.
9
We explored how methylcobalamin, a form of vitamin B12, impacts liver disease, particularly in the context of cholestatic liver failure. The study utilized high-throughput screening to identify methylcobalamin as a specific inhibitor of gasdermin E (GSDME), a protein that plays a key role in pyroptotic cell death—a form of inflammatory cell death contributing to liver damage.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
8
We explored the potential of an engineered yeast, S. cerevisiae-pYD1-ScFv-AFB1, in addressing liver damage caused by aflatoxin B1 (AFB1), a known cancer risk factor. Using a mouse model, we treated subjects with this specialized yeast for four weeks.
The results showed that the engineered yeast significantly reduced inflammation and cellular damage in the liver, and improved antioxidant capacity. Additionally, it helped repair the intestinal barrier disrupted by AFB1. These findings suggest it may offer a new way to combat AFB1 toxicity.
The results showed that the engineered yeast significantly reduced inflammation and cellular damage in the liver, and improved antioxidant capacity. Additionally, it helped repair the intestinal barrier disrupted by AFB1. These findings suggest it may offer a new way to combat AFB1 toxicity.
8
Saccharomyces-driven protection against liver toxicity
We explored how sophorolipids, produced by Saccharomyces cerevisiae using banana peels, could guard against liver damage caused by the chemotherapy drug doxorubicin (DOX). In our study with male Wistar rats, we compared the effects of sophorolipid treatment against DOX alone.
The results showed that applying sophorolipids improved liver function and adjusted key markers related to oxidative stress and inflammation. In essence, the sophorolipids appeared to offer protection against the harmful effects of DOX on the liver.
The results showed that applying sophorolipids improved liver function and adjusted key markers related to oxidative stress and inflammation. In essence, the sophorolipids appeared to offer protection against the harmful effects of DOX on the liver.
9
We explored the intriguing question of whether vitamin B12 can provide a protective effect against liver damage caused by acetaminophen, a common painkiller known for its potential hepatotoxicity. In our study, we used male Wister rats and organized them into three groups: one receiving acetaminophen, another treated with vitamin B12, and a control group given distilled water. Each group was administered their respective treatments for a week before we evaluated their liver health.
Our findings indicate that vitamin B12 supplementation significantly improved hepatic health in the rats exposed to acetaminophen. We observed a notable reduction in liver enzyme levels, which is a key marker of liver damage. Additionally, vitamin B12 helped boost antioxidant levels in the body, compensated for a decline in tissue glutathione, and reduced harmful inflammatory markers such as TNF-α and interleukin-6.
Overall, the results of our study suggest that vitamin B12 effectively mitigates acetaminophen-induced liver toxicity by enhancing liver function and reducing inflammation. This insight opens up interesting avenues for considering vitamin B12 as a supportive treatment in managing liver health in cases of acetaminophen exposure.
Our findings indicate that vitamin B12 supplementation significantly improved hepatic health in the rats exposed to acetaminophen. We observed a notable reduction in liver enzyme levels, which is a key marker of liver damage. Additionally, vitamin B12 helped boost antioxidant levels in the body, compensated for a decline in tissue glutathione, and reduced harmful inflammatory markers such as TNF-α and interleukin-6.
Overall, the results of our study suggest that vitamin B12 effectively mitigates acetaminophen-induced liver toxicity by enhancing liver function and reducing inflammation. This insight opens up interesting avenues for considering vitamin B12 as a supportive treatment in managing liver health in cases of acetaminophen exposure.
7
We explored the connection between high levels of Vitamin B12 and various health conditions, particularly focusing on liver disease. Our study involved analyzing medical records from 3,511 patients who had elevated serum Vitamin B12 levels over a year at King Salman Medical City in Madinah.
One significant finding was that a notable percentage of patients with elevated B12 levels also had diabetes mellitus, often linked to the use of Vitamin B12 as a supplement. Additionally, we observed associations with other health issues, including liver diseases among patients. However, the relationship between high B12 levels and liver disease was not isolated or definitively established; other factors played a role in these patients' health.
While the study did indicate a correlation between high Vitamin B12 levels and certain comorbidities, including liver conditions, further investigation is recommended to clarify the effects of Vitamin B12 treatment specifically on liver disease, as our findings were not conclusive. Thus, while we found that high serum levels of Vitamin B12 were prominent among patients with liver disease, we cannot definitively credit the treatment itself as a beneficial factor in this context.
One significant finding was that a notable percentage of patients with elevated B12 levels also had diabetes mellitus, often linked to the use of Vitamin B12 as a supplement. Additionally, we observed associations with other health issues, including liver diseases among patients. However, the relationship between high B12 levels and liver disease was not isolated or definitively established; other factors played a role in these patients' health.
While the study did indicate a correlation between high Vitamin B12 levels and certain comorbidities, including liver conditions, further investigation is recommended to clarify the effects of Vitamin B12 treatment specifically on liver disease, as our findings were not conclusive. Thus, while we found that high serum levels of Vitamin B12 were prominent among patients with liver disease, we cannot definitively credit the treatment itself as a beneficial factor in this context.
5
We sought to understand how vitamin B12 levels are affected by liver conditions, particularly focusing on non-alcoholic fatty liver disease (NAFLD). In a cross-sectional study involving 1,195 patients, we measured vitamin B12 levels and assessed liver conditions through techniques such as vibration-controlled transient elastography and ultrasonography.
Our findings indicated that vitamin B12 levels were notably lower in patients diagnosed with NAFLD compared to those with other chronic liver diseases. Specifically, the median B12 levels were 289 pg/mL in the NAFLD group versus 313 pg/mL in the others, highlighting a significant difference. We discovered a negative correlation between B12 levels and hepatic steatosis, suggesting that higher fat buildup in the liver corresponds to lower vitamin B12 levels.
Interestingly, we also observed that vitamin B12 levels increased with higher liver stiffness and were particularly significant in patients at the cirrhosis stage. This indicates that while vitamin B12 is reduced with higher steatosis levels, it does not render it ineffective or beneficial as a treatment, since patients with more advanced liver fibrosis generally had higher B12 levels.
Overall, our study enhances the understanding of the relationship between vitamin B12 and liver disease, showing that while there are fluctuations in B12 based on liver condition severity, it does not support the premise of using vitamin B12 as a treatment method for liver diseases.
Our findings indicated that vitamin B12 levels were notably lower in patients diagnosed with NAFLD compared to those with other chronic liver diseases. Specifically, the median B12 levels were 289 pg/mL in the NAFLD group versus 313 pg/mL in the others, highlighting a significant difference. We discovered a negative correlation between B12 levels and hepatic steatosis, suggesting that higher fat buildup in the liver corresponds to lower vitamin B12 levels.
Interestingly, we also observed that vitamin B12 levels increased with higher liver stiffness and were particularly significant in patients at the cirrhosis stage. This indicates that while vitamin B12 is reduced with higher steatosis levels, it does not render it ineffective or beneficial as a treatment, since patients with more advanced liver fibrosis generally had higher B12 levels.
Overall, our study enhances the understanding of the relationship between vitamin B12 and liver disease, showing that while there are fluctuations in B12 based on liver condition severity, it does not support the premise of using vitamin B12 as a treatment method for liver diseases.
References
- Huang H, Li Z, Qi Z, Ma L, Hu G, et al. Engineered S. cerevisiae-pYD1-ScFv-AFB1 mitigates aflatoxin B1 toxicity via bio-binding and intestinal microenvironment repair. Food Chem Toxicol. 2025;196:115232. 10.1016/j.fct.2024.115232
- Abdel-Latif GA, Al-Kashef AS, Nooman MU, Khattab AEA, Gebril SM, et al. The mechanistic interplay between Nrf-2, NF-κB/MAPK, caspase-dependent apoptosis, and autophagy in the hepatoprotective effects of Sophorolipids produced by microbial conversion of banana peels using Saccharomyces cerevisiae against doxorubicin-induced hepatotoxicity in rats. Food Chem Toxicol. 2023;182:114119. 10.1016/j.fct.2023.114119
- Abdel-Tawwab M, Khalil RH, Younis NA, Abo Selema TAM, Saad AH, et al. Saccharomyces cerevisiae supplemented diets mitigate the effects of waterborne cadmium toxicity on gilthead seabream (Sparus aurata L.): growth performance, haemato-biochemical, stress biomarkers, and histopathological investigations. Vet Res Commun. 2024;48:69. 10.1007/s11259-023-10176-0
- Cattaneo L, Lopreiato V, Piccioli-Cappelli F, Trevisi E, Minuti A. Effect of supplementing live Saccharomyces cerevisiae yeast on performance, rumen function, and metabolism during the transition period in Holstein dairy cows. J Dairy Sci. 2023;106:4353. 10.3168/jds.2022-23046
- Xu W, Wang Y, Cui S, Zheng Q, Lin Y, et al. Methylcobalamin protects against liver failure via engaging gasdermin E. Nat Commun. 2025;16:1233. 10.1038/s41467-024-54826-6
- Abu-Zahab ZA, Qureshi H, Adham GM, Elzefzafy WM, Zalam SS, et al. Frequency of comorbid diseases with high serum Vitamin B12 levels in patients attending King Salman Medical City (KSAMC), at Madinah. Int J Health Sci (Qassim). 2025;19:15.
- Espina S, Casas-Deza D, Bernal-Monterde V, Royo-Esteban A, García-Sobreviela MP, et al. Unraveling the Association of Liver Steatosis and Fibrosis with Vitamin B12: A Cross-Sectional Study. Metabolites. 2024;14. 10.3390/metabo14110618
- Roy A, Trigun SK. The restoration of hippocampal nerve de-myelination by methylcobalamin relates with the enzymatic regulation of homocysteine level in a rat model of moderate grade hepatic encephalopathy. J Biochem Mol Toxicol. 2024;38:e23695. 10.1002/jbt.23695
- Pai SL, Torp KD, Insignares VC, DeMaria S, Giordano CR, et al. Use of hydroxocobalamin to treat intraoperative vasoplegic syndrome refractory to vasopressors and methylene blue during liver transplantation. Clin Transplant. 2024;38:e15271. 10.1111/ctr.15271
- Liu K, Chen Y, Chen J, Chen W, Sun X, et al. Genetically determined circulating micronutrients and the risk of nonalcoholic fatty liver disease. Sci Rep. 2024;14:1105. 10.1038/s41598-024-51609-3
- Boachie J, Zammit V, Saravanan P, Adaikalakoteswari A. Metformin Inefficiency to Lower Lipids in Vitamin B12 Deficient HepG2 Cells Is Alleviated via Adiponectin-AMPK Axis. Nutrients. 2023;15. 10.3390/nu15245046
- Oula JO, Mose JM, Waiganjo NN, Chepukosi KW, Mitalo NS, et al. Vitamin B12 blocked Trypanosoma brucei rhodesiense-driven disruption of the blood brain barrier, and normalized nitric oxide and malondialdehyde levels in a mouse model. Parasitol Int. 2023;96:102775. 10.1016/j.parint.2023.102775
- Ujianti I, Sianipar IR, Prijanti AR, Hasan I, Arozal W, et al. Effect of Roselle Flower Extract ( Linn.) on Reducing Steatosis and Steatohepatitis in Vitamin B12 Deficiency Rat Model. Medicina (Kaunas). 2023;59. 10.3390/medicina59061044
- Ahmed Mohammed R, Fadheel QJ. Hepatoprotective Effect of Vitamin B12 in Acetaminophen Induce Hepatotoxicity in Male Rats. Arch Razi Inst. 2023;78:419. 10.22092/ARI.2022.359353.2408
