Abstract

The efficacies of two nutritional factors, folic acid and vitamin B 12, were assessed in this study against arsenic-induced islet cellular toxicity. Rats were divided into four groups consisting of five rats in each group: Group A, control; Group B, arsenic-treated; Group C, arsenic+folic acid; and Group D, arsenic+folic acid+vitamin B 12. The dose of arsenic, folic acid and vitamin B 12, respectively, was 3 mg, 36 μg and 0.63 μg kg −1 body weight day −1 for 30 days. Results showed that, compared to control group, there was a significant increase in the levels of nitric oxide (NO), malondialdehyde (MDA) and hydroxyl radical (OH −) formation in the pancreatic tissue of arsenic-treated rats, while the activity of antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT), and cellular content of antioxidant glutathione (GSH) were low in these animals. The serum level of tumor necrosis factor-α (TNF-α) and IL-6 was significantly high in these animals. Light microscopic examination showed a marked fall in the number of islet cells. Concomitant administration of either folic acid or folic acid and vitamin B 12 with arsenic significantly restored all these parameters. Although folic acid alone could not restore the normal level of TNF-α and IL-6, combined folic acid and vitamin B 12 could restore it. Folic acid and vitamin B 12 combined also could recover islet cell count. These results suggest that folic acid+vitamin B 12 are capable of reducing arsenic-induced cellular oxidative and inflammatory toxic changes. Thus, supplement with vitamin B 12+folic acid may be predicted as a possible nutritional management strategy against arsenic-induced toxicity.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.