Drugs online research references
Drug Chem Toxicol. 1998 May;21(2):163-79.
Preclinical toxicological evaluation of sertraline hydrochloride.
Davies TS, Klowe WM.
Pfizer Central Research, Groton, CT 06340, USA.
The toxicity profile of the antidepressant drug sertraline was determined in a series of preclinical studies in mice, rats, rabbits and dogs. Acute, subchronic, reproductive, chronic and carcinogenicity studies were conducted by the oral route. The highest doses tested in these studies were the maximum tolerated doses based on clinical signs, decreased food consumption, body weight effects, organ weight changes or clinical/anatomical pathology findings. Genetic toxicity studies were also performed. The liver was identified as a target organ in the mouse, rat and dog. The observed liver findings were consistent with hepatic xenobiotic-metabolizing enzyme induction and included hepatomegaly, hepatocellular hypertrophy, slightly increased serum transaminase activity and proliferation of smooth endoplasmic reticulum. Hepatocellular fatty change, a minimal toxic effect, was seen in mice and rats. There was no teratogenicity in studies conducted at maternally toxic doses in rats and rabbits. Decreased neonatal survival and growth observed in these studies have been previously reported in reproduction studies with other serotonin reuptake inhibitors. Sertraline was not genotoxic in an extensive battery of tests. Carcinogenicity tests were negative in rats, while benign liver tumors were slightly increased in drugtreated male mice. Liver tumors were considered secondary to the enzyme inducing potential of sertraline and not indicative of human risk.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9598298&dopt=Abstract
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J Affect Disord. 1998 May;49(2):141-4.
The SSRI antidepressants: exploring their "other" possible properties.
Andrews W, Parker G, Barrett E.
Psychiatry Unit, Prince of Wales Hospital, Sydney, Australia.
BACKGROUND: Anecdotal reports suggest that the SSRIs may have important properties in addition to their antidepressant effects, possibly modifying mediating variables that dispose to and maintain depression. This preliminary study seeks to identify any such potential variables. METHODS: Fifty three subjects who had reported substantial general benefit to their clinician after treatment with an SSRI were requested to retrospectively rate change across a range of constructs assessed by questionnaire. RESULTS: Differential effects were identified. Irritability, trait depression, worry and neuroticism scores showed the most marked improvement, with cognitive style components also showing significant positive change. Equally importantly, there was no evidence of a positive response bias across all constructs. CONCLUSION: We suggest that the SSRIs may act as "antiworry" agents and reduce irritability, neuroticism and dysfunctional attributions. LIMITATIONS: Our study was retrospective and relied on self-report by volunteer patients who had been previously depressed. The study design cannot exclude the possibility that improvement reported on a number of measures may have been due to the amelioration of residual depression. CLINICAL RELEVANCE: The SSRIs, recognised as having antidepressant and anti-obsessional properties, may also have the capacity to lower irritability, worrying and neuroticism. This capacity could be useful per se but may, in addition, reduce the occurrence and duration of depressive episodes, particularly by reducing "anxious worrying".
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9609678&dopt=Abstract
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Pharmacol Biochem Behav. 1998 May;60(1):83-90.
Cocaine and selective monoamine uptake blockers (sertraline, nisoxetine, and GBR 12935) prevent the d-fenfluramine-induced head-twitch response in mice.
Darmani NA.
Department of Pharmacology, Kirksville College of Osteopathic Medicine, MO 63501, USA.
Serotonin release subsequent to 5-HT precursor loading mainly occurs via exocytosis. Acute cocaine or sertraline administration promote the ability of 5-HT precursors (e.g. L-tryptophan) to induce the 5-HT2A receptor-mediated head-twitch response (HTR) in rodents. The 5-HT releaser, d-fenfluramine, at behaviorally active doses, can induce the head-twitch response in rodents by releasing cytoplasmic 5-HT via the serotonin uptake carrier working in reverse. The purpose of the present study was to utilize the d-fenfluramine-induced HTR to determine the serotonergic and nonserotonergic components of cocaine's actions on the d-fenfluramine-sensitive pool of cytoplasmic 5-HT. Because a dramatic differential potentiation in HTR frequency is obtained when cocaine is administered prior relative to after L-tryptophan injection, the effects of varying doses of cocaine and the selective serotonin (sertraline), dopamine (DA) (GBR 12935), and norepinephrine (NE) (nisoxetine) uptake blockers were investigated on the d-fenfluramine-induced behavior in two experimental protocols. Thus, each uptake inhibitor was administered either 10 min following (protocol 1) or 10 min prior to (protocol 2) d-fenfluramine injection. All the tested uptake inhibitors attenuated the d-fenfluramine-induced HTR in a dose-dependent manner in both experimental protocols. However, their order of potency in either protocol 1 (nisoxetine > GBR 12935 > cocaine > sertraline) or protocol 2 (cocaine > GBR 12935 > nisoxetine = sertraline) does not agree with in vitro affinity of these drugs for the 5-HT transporter. In addition, the potency order for cocaine and nisoxetine in protocol 1 was significantly reversed in protocol 2. The inhibitory effects of the cited drugs on the d-fenfluramine-induced HTR are discussed in terms of: 1) high doses of selective monoamine uptake blockers may not exhibit as much selectivity for their target uptake sites as indicated by in vitro tests; and 2) possible pharmacokinetic interactions between d-fenfluramine and the monoamine uptake blockers.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9610928&dopt=Abstract
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