Table 3.
In vivo interventional studies.
| Biological and Exposure Model | Intervention (substance/dose) | Effects/proposed mechanism | References |
|---|---|---|---|
| Wistar rats, 5.55 mg/kg/day AsIII (ip) for 30 days | N-acetylcysteine, 1 mmol/kg/day (og)for final 7 days of AsIII exposure | Nacetylcysteine's anti-oxidant properties reversed iAs-induced hepatic ROS-mediated toxicity, restored lower liver glycogen levels, and reversed hypoglycemia | (63) |
| Wistar rats, 5.55 mg/kg/day AsIII (ip) for 30 days | Melatonin, 10 mg/kg/day (og) for final 5 days of AsIII exposure | Melatonin's anti-oxidant properties reversed iAs-induced reductions in superoxide dismutase and catalase activities in the liver and kidney. | (97) |
| Wistar rats, 5.55 mg/kg/day AsIII (ip) for 21 days | Methionine, 0.8% of food supplement for final 5 days of AsIII exposure | Methionine treatment may have enhanced methylation of iAs reduced its toxicity, reversed hypoglycemia, reversed the iAs-induced reduction in liver pyruvic acid, and partially reversed the reduction in liver glycogen levels. | (62) |
| Swiss-albino mice, 3 mg/kg/day AsIII (og) for 12 weeks | (6)-gingerol, 50–75 mg/kg body weight/day (og) for 3 weeks after AsIII exposure | (6)-gingerol administration restored iAs-induced hyperglycemia to normoglycemia, decreased iAs deposition in the pancreas and liver, and restored liver antioxidant activities. | (59) |
| Wistar rats, 8 mg/kg/day As2O3 (og) from GD 6 to postnatal day 42 | Taurine, 150 mg/kg/day (og) from GD 6 to postnatal day 42 | Taurine reversed iAs-induced autophagosome formation, iAs-induced decrease in Nrf2 protein levels, and iAs-induced ROS accumulation in the pancreas. | (56) |
| Wistar rats, 8 mg/kg/day As2O3 (og) from GD 6 to postnatal day 42 | Taurine, 150 mg/kg/day (og) from GD 6 to postnatal day 42 | Taurine reversed iAs-induced TNF-α expression and markers of pyroptosis and inflammation in the pancreas. | (71) |
| Pregnant LM/Bc/Fnn mice, 9.6 mg/kg AsIII (ip), at GD 7.5 and GD 8.5 | Sodium selenate, 0.5 mg/kg (og) daily from GD 0.5 to GD 10.5 | Sodium selenite decreased the number of fetuses with neural tube defects. | (45) |
| Pregnant LM/Bc/Fnn mice, 9.6 mg/kg AsIII (ip), at GD 7.5 and GD 8.5 | L-Methionine, 70 mg/kg (og) daily from GD 0.5 to GD 10.5 | L-Methionine decreased the number of fetuses with neural tube defects. | (45) |
| Pregnant LM/Bc/Fnn mice, 9.6 mg/kg AsIII (ip), at GD 7.5 and GD 8.5 | N-acetylsysteine, 200 mg/kg (og) daily from GD 0.5 to GD 10.5 | N-acetylsysteine decreased the number of fetuses with neural tube defects but did not affect FPG or maternal circulating insulin | (45) |
| Pregnant LM/Bc/Fnn mice, 9.6 mg/kg AsIII (ip), at GD 7.5 and GD 8.5 | N-tert-Butyl-α-phenylnitrone,40 mg/kg (ip) on GD 7.5 and GD 8.5 | N-tert-Butyl-α-phenylnitrone decreased the number of fetuses with neural tube defects and significantly increased the rate of fetal resorption | (45) |
| Pregnant LM/Bc/Fnn mice, 9.6 mg/kg AsIII (ip), at GD 7.5 and GD 8.5 | LinBit insulin pellet implanted from GD 2.5–3.5 | LinBit decreased the number of fetuses with neural tube defects, decreased FPG, and increased matermal circulating insulin | (45) |
| C57BL/6J mice, 100 ppb AsIII (dw) for 24 weeks | Folate, 10 mg/kg of food supplement for 24 weeks | High folate supplementation improved iAs-induced insulin resistance and stimulated iAs metabolism in females. | (75) |
| Wistar rats, 5 mg/kg/day (og), for 30 days | Curcumin, 15 mg/kg/day (og), 30 days | Curcumin supplementation prevented iAs-induced changes in serum markers of hepatic and renal function. | (65) |