Arsenic and nicotine co-exposure lead to some synergistic effects on oxidative stress and apoptotic markers in young rat blood, liver, kidneys and brain

Abstract

Arsenic and nicotine exposure has been a major health concern globally. Individually both these toxicants increase the risk to various diseases including cancers. However, limited information exists on the co-exposure. In this study, we evaluate the effects of their individual and combined exposure and if co-exposure to these toxicants might have a synergism or antagonism. Male rats were exposed to a very low dose of arsenic (25 ppm in drinking water) or nicotine (0.25 mg/kg, sub-cutaneously) for a period of 5 months and post exposure various biochemical variables indicative of oxidative stress and apoptosis evaluated. Almost all glutathione linked enzymes showed marked alteration in individual as well as co-exposure treated groups. While serum creatinine and apoptosis indicator, lactate dehydrogenase (LDH) were significantly increased in both treatments, an additive effect was noted in co-exposure group. A similar trend was also seen in brain and liver but not in kidneys. Gene expression studies showed marked reduction in catalase, Cu-Zn SOD, GST, there was a significant up regulation in Bax, caspase 3 in various tissues along with urinary 8-OHdG levels, indicative of DNA damage and apoptosis. Interestingly, a decrease in liver arsenic concentration was noted in co-exposed group compared to arsenic alone exposed group. In conclusion, the present study suggests that arsenic and nicotine exhibited significant toxicity during individual exposure whereas co-exposure to these toxins showed variable conditions (indicative of both synergism and antagonism) in male rats.

RETRACTED ARTICLE: Sulforaphane potentially attenuates arsenic-induced nephrotoxicity via the PI3K/Akt/Nrf2 pathway in albino Wistar rats

“…In the current study, Ar administration significantly reduced enzymatic antioxidants such as SOD, CAT, GPx, GST, and GR in comparison to controls. This result was well in line with an earlier report by Jain et al ( 2015 ), who observed lower levels of enzymatic antioxidants in arsenic-treated rat kidneys. Similarly, Gong et al ( 2015 ) observed a reduction in enzymatic antioxidants in Ar-treated rats, mainly due to oxidative stress and unpaired electrons in the renal tissue.…”

“…One organ typically affected by Ar-induced ROS production is the kidney (Prabu and Muthumani 2012 ). In the current study, a notable increase in ROS was found in the blood and renal tissue of Ar-intoxicated rats versus controls, which confirms earlier reports (Jain et al 2015 ). This may be due to the induction by Ar of a complex chain of one-electron reduction of molecular oxygen, which first leads to the formation of superoxide radicals (O 2 ) in the kidney.…”

Alteration in thiols homeostasis, protein and lipid peroxidation in renal tissue following subacute oral exposure of imidacloprid and arsenic in Wistar rats

“…Simultaneous exposure of both the toxicants produced more pronounced increase in oxidation of membrane lipids (401.2%) and proteins (40.0%) of renal tissue compared to control as well as exposure of either toxicant ( Table 1 ). These observations are in accordance with the observations reported with co-exposure of metals and insecticides to rats [ 39 , 41 , 46 ].…”

“…Co-exposure to IMI and arsenic produced more pronounced fall in TTH level (63.8%) in renal tissue as compared to control ( Table 1 ). Similar decline in TTH level have also been reported in different visceral organs in arsenic exposed rats [ [46] , [47] , [48] ].…”

Oxidative/ Nitrosative Stress, 8-OHdG and MMP-9: The Possible Co-Links and Early Sign of Arsenic Induced Urinary Bladder Carcinogenesis in Experimental Rats

“…However some in-vitro and in-vivo studies suggested that carcinogenic potency of DMA is more than that of sodium arsenite. 52,53 Our results although in some disagreement with available literature and observed arsenic (III) to be more carcinogenic than DMA possibly due to deteriorative effects of DMA via oral route.…”