Potential Utility Of 2-(2-(5-Nitro-1-H-Benzo[D]Thiazole-2-Yl) Vinyl)-4H-6-Chloro Chromene-4-One to Mitigate the Toxic Impact of Xenobiotics in Mammals

Abstract

This research aimed to investigate the individual and combined effects of two substances, 2-(2-(5-nitro-1-H-benzo[d]thiazole-2-yl) vinyl)-4H-6-Chloro Chromene-4-one referred as S1 and 2-(2-(5-nitro-1-H-benzo[d]thiazole-2-yl) vinyl)-4H Chromene-4-one referred as S2, on the survival of rats and the characteristics of total mRNA involved in molecular genetic processes in these animals. The study was conducted using Wistar Han (SPF) rats. S1, when administered at doses of 13 and 0.013 mg/kg body weight, which correspond to 1/100 and 1/100000 of the lethal dose (DL50), did not result in any clinical signs of intoxication in the rats. S1 was found to increase the level of hybridization in mRNA preparations obtained from both rat liver and blood cells. This effect was more pronounced at the higher dose of 13 mg/kg body weight compared to the lower dose of 0.013 mg/kg body weight. In contrast, when rats were exposed to S2 at a dose of 540 mg/kg body weight, equivalent to 1 DL50, pronounced intoxication was observed after 6 hours, leading to a 40% mortality rate among the animals. Interestingly, when rats were first intraperitoneally administered S1, followed by oral administration of S2 at the same doses (after 24 hours), the rats remained viable. Furthermore, the degree of hybridization of cytoplasmic mRNA with [ɑ32P]-cDNA only showed a slight decrease by the end of the second day. By the third day, the overall condition of the animals had returned to normal. This combined treatment also resulted in an increase in the degree of hybridization between the mRNA molecules isolated from control rats and [ɑ32P]-cDNA obtained from the experimental group. In summary, this study suggests that S1, even at higher doses, does not induce intoxication in rats and can enhance mRNA hybridization. Furthermore, when administered before S2, it appears to protect the rats from the toxic effects of S2, as indicated by their improved survival and the recovery of molecular genetic processes.