Nephrotoxic and hepatotoxic effects of triclosan and chlorhexidine in rats

Chow, A.Y.K.; Hirsch, G. H.; Buttar, Harpal S.

doi:10.1016/0041-008x(77)90191-0

Cited by 30 publications

(7 citation statements)

References 17 publications

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“…Through utilizing our previously developed methods, concentrations of BZK, BZT and CHX in blood, lung, liver and kidney in rats were determined following a dose of 15 mg kg −1 intravascularly or 250 and 1250 mg kg −1 orally. Lung, liver and kidney were selected as tissue samples because these organs have been reported as affected tissues in human poisoning cases and in animal experiments (Xue et al , 2004a, b; Tiess and Nagel, ; Mucklow, ; Chow et al , ). The individual levels in blood and tissues at 24 h after administration were plotted.…”

Section: Resultsmentioning

confidence: 99%

Comparative study on toxic effects induced by oral or intravascular administration of commonly used disinfectants and surfactants in rats

Yang

Zhang

Tang

et al. 2011

J of Applied Toxicology

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Accidental ingestion or injection of household products sometimes occurs due to their accessibility, but the toxic manifestations have not been well characterized when they are internally administered. The aim of this study was to investigate the toxic effects induced by ingestion or injection of different ionic surfactants and disinfectants in rats. The test drugs involved benzalkonium and benzethonium (BZK and BZT, both cationic surfactants used as disinfectants), alkyldiaminoethylglycine (AEG, an amphoteric surfactant used as a disinfectant), linear alkylbenzenesulfonate (LAS, an anionic surfactant), polyoxyethylene cetylether (PEC, a nonionic surfactant), chlorhexidine (CHX, not a surfactant but a disinfectant) and saline (control). Male Sprague-Dawley rats were administered one of the test drugs orally (p.o.), intravenously (i.v.) or intraarterially (i.a.). The fatal effects appeared rapidly (<30 min) in i.v.-administered rats, while taking hours (>5 h) in i.a./p.o.-administered rats after a dose of around LD(50) , although the progress and degree of toxic effects varied among the drugs tested. In intravascular administration, BZK and BZT were fatal at doses of 15-20 mg kg(-1) . Higher concentrations in lung and kidney than in blood were determined. CHX showed a high toxic effect compared with cationic surfactants. The rats administered anionic (LAS) or amphoteric (AEG) surfactant died in less than 24 h at doses over 100 mg kg(-1) . In p.o. administration, the toxic effects were concentration/dose-dependent, and all rats administered high doses of surfactants except for PEC died at 5-20 h. The overall toxic ranks could be: cationic surfactant/CHX> anionic/amphoteric surfactant > nonionic surfactant.

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Section: Resultsmentioning

confidence: 99%

Comparative study on toxic effects induced by oral or intravascular administration of commonly used disinfectants and surfactants in rats

Yang

Zhang

Tang

et al. 2011

J of Applied Toxicology

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“…CHX in the whole blood and tissue samples was extracted by solid phase extraction and determined by HPLC utilizing our previously described method. 16 Lung, liver and kidney were selected as tissue samples because: (1) these organs have been reported as affected tissues in human poisoning cases and in animal experiments 5,22 and (2) the detected CHX levels were higher than those in other tissues in our preliminary study (data not shown), which would allow quantification of lower CHX levels at later time.…”

Section: Methodsmentioning

confidence: 99%

Acute pulmonary toxic effects of chlorhexidine (CHX) following an intratracheal instillation in rats

et al. 2011

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Chlorhexidine (CHX) is a cationic biguanide compound that has been widely used for disinfection of skin, mucous membranes, and medical instruments. Poisoning has been occurred occasionally due to its easy accessibility. Some fatal cases developed acute respiratory distress syndrome (ARDS) from aspiration of CHX directly into the lung. There is no preclinical information about the pulmonary toxicity of CHX available since the products of CHX are usually developed for disinfection by topical use. In this study, the acute pulmonary toxic effects of CHX following an intratracheal instillation in rats were investigated. Rats were exposed either to CHX at concentrations of 0.02% and 0.2% or to distilled water at a volume of 500 μl/kg b.w. CHX at concentration of 0.2% caused changes in hematological and biochemical values including white blood cell count (WBC), total protein (TP), albumin (ALB), lactate dehydrogenase (LDH), blood urea nitrogen (BUN) and creatinine (CRE), and induced inflammatory reactions including intra-alveolar edema and hemorrhages, as well as resulted in the target organ concentration in lungs at the level of about 1.0 μg/g and maintained for more than 1 week, when administered intratracheally in rats. The cytotoxic action of CHX might induce those detrimental reactions in rats.

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“…An early study by Lyman and Furia (), sanctioned by the Geigy Chemical Corporation, provided toxicological data on TCS in rats, concluding that TCS was neither acutely toxic (LD50 oral > 1000 mg kg −1 ) nor carcinogenic. Later, nephrotoxic effects of orally administered TCS in rats were reported by Chow et al (), in a study where the accumulation of p ‐aminohippurate (PAH) was estimated both in vivo and in vitro , using kidney slices to detect dose‐related inhibition. A 1989 review on the safety of TCS was published by DeSalva et al ().…”

Section: Toxicitymentioning

confidence: 99%

Triclosan: environmental exposure, toxicity and mechanisms of action

Dann

Hontela

2010

J of Applied Toxicology

746

431

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Triclosan [5-chloro-2-(2,4-dichlorophenoxy)phenol; TCS] is a broad spectrum antibacterial agent used in personal care, veterinary, industrial and household products. TCS is commonly detected in aquatic ecosystems, as it is only partially removed during the wastewater treatment process. Sorption, biodegradation and photolytic degradation mitigate the availability of TCS to aquatic biota; however the by-products such as methyltriclosan and other chlorinated phenols may be more resistant to degradation and have higher toxicity than the parent compound. The continuous exposure of aquatic organisms to TCS, coupled with its bioaccumulation potential, have led to detectable levels of the antimicrobial in a number of aquatic species. TCS has been also detected in breast milk, urine and plasma, with levels of TCS in the blood correlating with consumer use patterns of the antimicrobial. Mammalian systemic toxicity studies indicate that TCS is neither acutely toxic, mutagenic, carcinogenic, nor a developmental toxicant. Recently, however, concern has been raised over TCS's potential for endocrine disruption, as the antimicrobial has been shown to disrupt thyroid hormone homeostasis and possibly the reproductive axis. Moreover, there is strong evidence that aquatic species such as algae, invertebrates and certain types of fish are much more sensitive to TCS than mammals. TCS is highly toxic to algae and exerts reproductive and developmental effects in some fish. The potential for endocrine disruption and antibiotic cross-resistance highlights the importance of the judicious use of TCS, whereby the use of TCS should be limited to applications where it has been shown to be effective.

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Nephrotoxic and hepatotoxic effects of triclosan and chlorhexidine in rats

Cited by 30 publications

References 17 publications

Comparative study on toxic effects induced by oral or intravascular administration of commonly used disinfectants and surfactants in rats

Comparative study on toxic effects induced by oral or intravascular administration of commonly used disinfectants and surfactants in rats

Acute pulmonary toxic effects of chlorhexidine (CHX) following an intratracheal instillation in rats

Triclosan: environmental exposure, toxicity and mechanisms of action

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