Objective: This study was aimed to evaluate the effects of daily intake of vitamin C or selenium against deleterious effects of nicotine toxicity on pregnant albino rats. Materials and methods: Forty albino pregnant rats were equally distributed into four groups. Group A was considered as control. Group B was administered with nicotine dosed at 1 mg/kg body weight (bwt) daily for 7 weeks (wks) from 1st day of gestation until the postnatal 4 wks. Group C was treated with nicotine and vitamin C dosed at 1 mg/kg bwt orally for 7 wks, group D was treated with nicotine and sodium selenite dosed at 1 ug/100 g bwt concurrently for 7 wks. The levels of catalase (CAT), superoxide dismutase (SOD), protein carbonyl (PC) and thiobarbituric acid reactive substances (TBARS), were estimated in homogenates of the lung, kidney and liver. Histopathological studies using hematoxylin and eosin as well as immunohistochemical studies using p53 antibody were also done. Results: Nicotine significantly elevated the levels of TBARS and PC as compared to control rats. Groups C and D showed decrease in these levels significantly. CAT and SOD activities of group B were decreased significantly. Significant elevation of CAT and SOD activities was detected in both groups C and D. Vitamin C elevated the antioxidant enzymes activities to normal levels, however selenium administration improved these levels but still lower than those of group A. Expression of p53 was decreased in group B as compared to group A. Vitamin C completely reversed the expression of p53 as group A. However, group D did not showed any significant changes in expressions as compared to group B. Conclusion: It is concluded that vitamin C intake was useful than selenium in prevention against nicotine-induced oxidative stress including p53 expression in the lung, kidney and liver of pregnant rats. [J Adv Vet Anim Res 2016; 3(4.000): 321-331]

Substance P (SP) is colocalized with ACh in splanchnic nerves that innervate into adrenal medulla and the peptide has been shown to inhibit nicotinic agonists-induced catecholamine secretion. To elucidate the effects of SP on cytosolic Ca(2+) dynamics, the present study was conducted using fura-2-loaded isolated bovine adrenal chromaffin cells. Stimulation of the cells with nicotine (10-100mu-M) produced a rapid rise of cytosolic Ca(2+) concentration ([Ca(2+)]i), the peak level of which increased in a dose-dependent manner, followed by a gradual decay. In the presence of 10mu-M SP, the dose-response relationship of the peak levels shifted downward. Quantitative analyses implied that SP inhibits the nicotine-induced Ca(2+) influx in a noncompetitive manner. Nicotinic acetylcholine receptor is composed of two major functional domains: an agonist-binding site and an ionophore or channel domain. Agonist binding activates ionophore / channel domain and causes mainly Na(+) influx. This Na(+) influx depolarizes the cell and activates voltage-dependent Ca(2+) channels. Based on this fact, the present results indicate that SP dose not block nicotine binding sites but interferes with other sites of nicotinic receptor / channel molecule, most probably a channel domain. It was suggested that SP colocalized with ACh in splanchnic nerves functions as a physiological modulator of catecholamine secretion by non-competitively suppressing ACh-induced cytosolic Ca(2+) dynamics in bovine a

Objective: The present research was conducted to evaluate the negative effects of nicotine powder on the blood physiology, and biochemical and histological alterations of Labeo rohita. Materials and Methods: Fish were divided into four groups (1–4). Fish groups 2, 3, and 4 were exposed to different concentrations of nicotine, such as 0.75, 1.25, and 1.75 mg/l, while group 1 acted as a control. To find out the long-term impact of nicotine on body physiology, we conducted a 42-day experiment. After the completion of the experiment, hematology, biochemical assays, and histology were done. Results: Results revealed a considerable increase in HGB, red blood cells, WBCs, hematocrit, mean corpuscular volume, red cell distribution width -SD, procalcitonin, neutrophils, lymphocytes, monocytes, triglycerides, total cholesterol, low-density lipoprotein, very low-density lipoprotein, alanine transaminase, aspartate aminotransferase, globulin, thyroid stimulating hormone, BUN, creatinine, and blood glucose levels, whereas mean corpuscular hemoglobin concentration, mean corpuscular hemoglobin, RDW, platelet, high-density lipoprotein, albumin, total proteins, and T3 levels were significantly (p ≤ 0.05) decreased in exposed fish as compared to control group fish. Histological alterations showed that exposure to smokeless nicotine causes deleterious and degenerative effects in the liver, kidney, and gills of exposed fish. Conclusion: Nicotine administration in fish results in adverse effects on different biochemical and hematological parameters and causes histological alterations in some vital organs of exposed fish. [J Adv Vet Anim Res 2024; 11(2.000): 463-473]