Antiapoptotic efficacy of folic acid and vitamin B₁₂ against arsenic‐induced toxicity

Abstract

Earlier, we proposed that the ability of folic acid and vitamin B₁₂ to preserve systemic and mitochondrial function after short-term exposure to arsenic may prevent further progression to more permanent injury and pathological changes leading to cell death. To elucidate its mechanism, the present study examined the antiapoptotic efficacy of folic acid and vitamin B₁₂ against short-term arsenic exposure-induced hepatic mitochondria oxidative stress and dysfunction. Sixteen to eighteen weeks old male albino rats weighing 140-150 × g were divided into five groups: Control (A), Arsenic-treated (B), Arsenic + folic acid (C), Arsenic +vitamin B₁₂ (D), and Arsenic + folic acid + vitamin B₁₂ (E). Data generated indicated that folic acid and vitamin B₁₂ separately or in combination can give significant protection against alterations in oxidative stress and apoptotic marker parameters and downstream changes in mitochondria, namely pro-oxidative (NO, TBARS, OH⁻) and antioxidative defense (SOD, CAT, GSH) markers, iNOS protein expression, mitochondrial swelling, cytochrome c oxidase and Ca²⁺-ATPase activity, Ca²⁺ content, caspase-3 activity. Additionally, results of hepatic cell DNA fragmentation, arsenic load of blood, hepatic tissue and urine, and histological observations, all strongly support that both these supplements have efficacy in preventing apoptotic changes and cellular damage. As the mechanisms of actions of both of these supplements are methylation related, a combined application was more effective. Results further reveal new molecular targets through which folic acid and vitamin B₁₂ separately or in combination work to alleviate one critical component of arsenic-induced liver injury: mitochondria dysfunction.

Acidithiobacillus ferrivorans SS3 presents little RNA transcript response related to cold stress during growth at 8 °C suggesting it is a eurypsychrophile

“…Cobalamin is a cobalt-coordinated tetra pyrrole and is used as an enzyme cofactor in prokaryotes. However, it has also been reported to restore the activity of other ROS scavenging proteins (Majumdar et al 2012; Chattopadhyay et al 2012) that were found in the genome, namely catalase (Acife_2431) and superoxide dismutase (Acife_1434). Its genomic production potentially includes three cobalt transporters (Acife_0490, Acife_1063, and Acife_2190), as well as the cobalamin biosynthesis proteins CobS (Acife_2993), CbiX (Acife_2081), and two copies of CbiA (Acife_1891 and Acife_3125).…”

Effects of folic acid administration on testicular ischemia/reperfusion injury in rats

“…In this regard, 74% increase in the sperm count in the men reported after administration of the FA. Also, FA (3 mg/day for 3 months) improved spermatozoa number and motility in infertile men 29 . FA could protect cells against damage caused by lead 32 .…”

“…However, Raigani reported FA supplementation did not ameliorate sperm quality in infertile men 28 . The FA successfully alleviated the SOD, GPx depletion and MDA elevation 29 . In this study, dose dependent increase observed on spermatozoa mobility, mortality (%) using different levels of the FA (2, 5 and 10 mg/kg) treated rat (Figures 2-3).…”

“…The FA (2, 5 and 10 mg/kg) significantly increased tissue SOD and GPx activity in I/R rat ( Table 1). Supplementation of the FA decreases the risk of heart and limb defects 26 and urinary tract anomalies [29][30] . The I/R injury in testis resulted in decrease in spermatogenesis 31 .…”

Cognition and biomarkers of oxidative stress in obstructive sleep apnea

“…Preliminary evidence indicates that folic acid and vitamin B12 have anti-apoptotic efficacy and the ability to preserve mitochondrial function (25). Furthermore, vitamin B11 deficiency has been associated with elevated concentrations of homocysteine in the plasma of elderly non-demented patients (26,27).…”