Nicotine administration to rats: Methodological considerations

Lc, Murrin; Ferrer, L.; Wy, Zeng; Nj, Haley

doi:10.1016/0024-3205(87)90020-8

Cited by 223 publications

(113 citation statements)

References 12 publications

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“…The gavage method used in the current investigation was performed in order to avoid the unpalatability of administering nicotine via drinking water. [17] The toxic effects of nicotine on renal function are well known, as emphasized in an early paper. [18] Methanol poisoning as a consequence of methylated spirits ingestion was published in communities resident in Papua New Guinea.…”

Section: Discussionmentioning

confidence: 99%

Renal Function in Male Sprague-Dawley Rats Concurrently Exposed to Long-Term Nicotine (3-{1-Methyl-2-Pyrrolidinyl}Pyridine) and Methylated Spirits (Methyl Alcohol)

2008

Renal Failure

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Abuse of nicotine and methylated spirits is a global problem. The current study determined the concurrent influence of nicotine and methylated spirits on renal hemodynamics. Two series of experimental protocols were designed: conscious and anesthetized vehicle loading. Conscious animals received nicotine (0.1 mg.kg -1 bwt, 0.26-0.30 mL), methylated spirits (1.0 g.kg -1 bwt, 0.26-0.30 mL), combined nicotine and methylated spirits, and control animals (water, 0.26-0.30 mL). Anesthetized animals were challenged with a continuous jugular infusion of 0.077M NaCl. Plasma nicotine concentration was significantly elevated in combined conscious treatments by comparison with animals infused nicotine alone. Plasma arginine vasopressin was significantly attenuated in combined conscious groups, and those infused methylated spirits alone. Aldosterone was elevated in all conscious groups. Both plasma ethanol and methanol concentrations were elevated in rats concurrently administered nicotine and methylated spirits compared with those given methylated spirits alone. Urinary Na + levels were significantly elevated in all anesthetized groups associated with attenuated aldosterone concentrations. Plasma nicotine concentrations were increased in combined treatments. Plasma ethanol levels were significantly reduced and elevated in rats concurrently exposed to nicotine and methylated spirits, respectively. The present study suggests that chronic exposure to methylated spirits alone and in combination with nicotine increases urinary Na + loss. The renal toxicity is manifested hypothetically via elevations in plasma nicotine and methanol concentrations. This implies that people who concurrently consume methylated spirits and smoke cigarettes have an increased risk of renal failure by being predisposed to fluid and electrolyte disturbances.

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Section: Discussionmentioning

confidence: 99%

Renal Function in Male Sprague-Dawley Rats Concurrently Exposed to Long-Term Nicotine (3-{1-Methyl-2-Pyrrolidinyl}Pyridine) and Methylated Spirits (Methyl Alcohol)

2008

Renal Failure

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“…In this study, we used nicotine osmotic minipumps at an infusion rate of 6 mg/kg per day in the mothers to produce nicotine levels quite similar to those achieved in heavy smokers (Murrin et al 1987, Lichtensteiger et al 1988. To our knowledge, there are a few experimental studies focusing on the effects of nicotine exposure exclusively during the early postnatal period.…”

Section: Introductionmentioning

confidence: 99%

Nicotine exposure affects mother's and pup's nutritional, biochemical, and hormonal profiles during lactation in rats

Oliveira¹,

Pinheiro²,

Santos-Silva³

et al. 2010

Journal of Endocrinology

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We have shown that maternal nicotine exposure during lactation has long-lasting effects on body adiposity and hormonal status of rat offspring. Here, we studied the nutritional and hormonal profiles in this experimental model. Two days after birth, osmotic minipumps were implanted in lactating rats divided into two groups: NICcontinuous s.c. infusions of nicotine (6 mg/kg per day) for 14 days and C -saline. Dams and pups were killed at 15 and 21 days of lactation. Body weight and food intake were evaluated. Milk, blood, visceral fat, carcass, and adrenal gland were collected. All the significant data were P!0 . 05. At the end of nicotine exposure (15 days), dams presented higher milk production, hyperprolactinemia, and higher serum highdensity lipoprotein cholesterol (HDL-C). Milk from NIC dams had higher lactose concentration and energy content. After nicotine withdrawal (21 days), dams showed lower food intake and hyperleptinemia. The 15-day-old NIC pups presented higher total body fat, higher HDL-C, serum leptin, serum corticosterone, and adrenal catecholamine content, but lower tyrosine hydroxylase protein levels. The 21-day-old NIC pups had higher body protein content and serum globulin. Thus, maternal nicotine exposure during lactation results in important changes in nutritional, biochemical, and hormonal parameters in dams and offspring. The pattern of these effects is clearly distinct when comparing the nicotineexposed group to the withdrawal group, which could be important for the programming effects observed previously.

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“…In the current study, we administered nicotine to pregnant Rhesus macaque monkeys throughout pregnancy until just before term, using continuous infusions of nicotine via osmotic minipumps, so as to avoid confounding effects of fluctuating drug levels and the associated incidence of fetal hypoxia/ischemia (Levin and Slotkin, 1998;Slotkin, 1992Slotkin, , 1999Slotkin, , 2004, carefully matching the dose rate so as to simulate the plasma levels of nicotine commonly associated with maternal smoking or with use of transdermal nicotine patches (Benowitz et al, 1990;Fredrickson et al, 1995;Isaac and Rand, 1972;Lichtensteiger et al, 1988;Luck et al, 1985;Murrin et al, 1987). Fetal brain regions, heart and lung were then examined for four families of biomarkers known to characterize neurodevelopmental deficits associated with nicotine exposure.…”

Section: Introductionmentioning

confidence: 99%

Effects of Prenatal Nicotine Exposure on Primate Brain Development and Attempted Amelioration with Supplemental Choline or Vitamin C: Neurotransmitter Receptors, Cell Signaling and Cell Development Biomarkers in Fetal Brain Regions of Rhesus Monkeys

Slotkin

Seidler

Qiao

et al. 2004

Neuropsychopharmacol

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Studies in developing rodents indicate that nicotine is a neuroteratogen that disrupts brain development by stimulating nicotinic acetylcholine receptors (nAChRs) that control neural cell replication and differentiation. We administered nicotine to pregnant Rhesus monkeys from gestational day 30 through 160 by continuous infusion, achieving maternal plasma levels comparable to those in smokers (30 ng/ml). Fetal brain regions and peripheral tissues were examined for nAChR subtypes, other neurotransmitter receptors, and indices of cell signaling and cell damage. Nicotine evoked nAChR upregulation, but with distinct regional disparities indicative of selective stimulatory responses. Similarly, indices of cell loss (reduced DNA), cell size and neuritic outgrowth (protein/DNA and membrane/total protein ratios) were distinct for each region and did not necessarily follow the rank order of nAChR upregulation, suggesting the involvement of additional mechanisms such as oxidative stress. We then attempted to offset the adverse effects of nicotine with standard dietary supplements known to interact with nicotine. By itself, choline elicited nicotine-like actions commensurate with its promotion of cholinergic neurotransmission. When given in combination with nicotine, choline protected some regions from damage but worsened nicotine's effects in other regions. Similarly, Vitamin C supplementation had mixed effects, increasing nAChR responses while providing protection from cell damage in the caudate, the brain region most susceptible to oxidative stress. Our results indicate that nicotine elicits neurodevelopmental damage that is highly selective for different brain regions, and that dietary supplements ordinarily thought to be neuroprotectant may actually worsen some of the adverse effects of nicotine on the fetal brain.

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Nicotine administration to rats: Methodological considerations

Cited by 223 publications

References 12 publications

Renal Function in Male Sprague-Dawley Rats Concurrently Exposed to Long-Term Nicotine (3-{1-Methyl-2-Pyrrolidinyl}Pyridine) and Methylated Spirits (Methyl Alcohol)

Renal Function in Male Sprague-Dawley Rats Concurrently Exposed to Long-Term Nicotine (3-{1-Methyl-2-Pyrrolidinyl}Pyridine) and Methylated Spirits (Methyl Alcohol)

Nicotine exposure affects mother's and pup's nutritional, biochemical, and hormonal profiles during lactation in rats

Effects of Prenatal Nicotine Exposure on Primate Brain Development and Attempted Amelioration with Supplemental Choline or Vitamin C: Neurotransmitter Receptors, Cell Signaling and Cell Development Biomarkers in Fetal Brain Regions of Rhesus Monkeys

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