YefenghongAugust 14, 2018
Tag: triclosan , TCS , Carcinogen
Triclosan (TCS) is widely applied in personal care products (such as toothpaste and cosmetics), consumer goods for daily use (such as fiber knitwear), medical supplies (such as dental consumables and medical fungicides), and household cleaning products as a broad-spectrum antimicrobial agent. TCS extensively exists in various environmental media due to the large amount of application, and it mainly enters water bodies through effluent discharge of sewage plants, to eventually enter the surface water, soil, and underground water. TCS can now be detected in the sewage treatment plant influent and effluent, sludge, rivers, estuaries, and sediments.
An article published on Science Translational Medicine recently also proves that TCS can have adverse effects on colonic inflammation and associated colon tumorigenesis through modulation of the gut microbiota and TLR4 signaling. Most of the studies were conducted on cells or animals, and it’s not clear whether such risks could happen to humans, however, the effects of TCS on human health cannot be ignored.
There has been a large number of studies exploring the possible toxic effects of TCS on living things. I’d like to summarize those study results here, in the hope of providing some help for your health management.
Enzyme and gene toxicity
TCS can produce toxic effects to organisms at molecular level. The toxic effects of TCS at enzyme and protein level manifest as the inhibitory effects on the antioxidant enzyme system in organisms through induction of oxidative stress, such as superoxide dismutase (SOD), malondialdehyde (MDA), aminopyrine N-demethylase (APND), catalase (CAT), and glutathione S-transferase (GST), and the effects on the cytochrome oxidase system of organisms, such as P450 and CYP1A. Furthermore, study also shows that TCS can affect the expression of the heat shock protein Hsp70. Its effects at the gene level manifest as TCS’ direct damage to DNA, and possible effect on DNA synthesis as an adduct, to interfere with the normal physiological inheritance function of DNA. Moreover, TCS can also produce toxic effects on organisms by interfering with the transduction of intracellular molecular signals.
Cytotoxic effect
Some studies show that TCS can promote the proliferation of cancer cells, such as human hepatoma cells, ovarian cancer cells, prostate cancer cells, and breast cancer cells. According to mechanism research, the effect of TCS on cancer cell proliferation may be that it regulates the expression of cyclin D1, P21 and Bax related with cell cycle and apoptosis via the estrogen/androgen-mediated signaling pathway, thus to promote cancer cell growth.
Reproductive system toxicity
TCS is structurally similar to estrogen, and it can bind to estrogen receptor (ER) by competing with endogenous estrogen, thus to directly affect the transcriptional activity of ER and cause estrogenic effect (or antiandrogenic effect). Study shows that TCS can accelerate the sexual maturity of female rats and increase weight of their womb, and advance birth canal opening of pregnant rats, while, TCS can reduce weight of male rats’ testis and prostate, etc., and significantly reduce gene expression of androgen-related protein and sterol producing enzyme, and reduce level of androgenic hormone in serum. TCS can accumulate in the epididymis of male rat, to cause its tissue form to change and affect the sperm morphology and quantity. TCS can also inhibit activity of estrogen sulfotransferase in sheep placenta and affect the placenta’s estrogen supply to the fetus.
Thyroid system toxicity
The endocrine disruption of TCS also manifests as the effects on the thyroid system of organisms. TCS can indirectly affect the metabolism of the thyroid system, for example, TCS can reduce the transcription level of thyroid hormone receptor alpha in organisms, or inhibit activity of T2 sulfotransferase, to affect the thyroid hormone-mediated growth and development. Besides the indirect effect on the metabolism of the thyroid system, TCS can also directly affect thyroid tissues and their hormone. According to research, TCS can cause the up-regulated expression of relevant genes of thyroid stimulating hormone (TSH) and sodium/iodide symporter (NIS) in zebrafish, and cause histomorphology distortion of thyroid.
Central nervous system toxicity
TCS can activate extrinsic apoptotic signaling pathway by inducing expression of FasR and caspase-8, thus to cause the apoptosis of neurons in brain, however, more explorations are needed as to whether TCS can affect the central nervous system via other pathways. Triclocarban (TCC) that is very similar to TCS in structure can affect brain tissue development by strengthening overexpression of aromatase AroB induced by exogenous estrogen (Chung, 2011), therefore, whether TCS can affect brain tissue though a mechanism similar to TCC still needs to be proved by study.
To sum up, TCS can affect living things at molecular and cellular levels, produce enzyme and gene toxicity, and cause the mutation and canceration of tissues and organs of organisms. Furthermore, TCS significantly interferes with internal secretion of organisms, and can damage homeostasis of living things by affecting reproductive and development systems, thyroid system, and central nervous system, however, relevant molecular mechanisms still need to be further studied.
In fact, TCS and disinfectants that contain other antibiotics are used far more often in hospitals than other environments. Considering that over 98% infants are born in hospital, the contact with TCS at fetal stage, perinatal stage and after birth may affect the health of fetuses/infants. Therefore, it’s very important to study carefully the effects of TCS on microbial construction and composition.
References:
1.A common antimicrobial additive increases colonic inflammation and colitis-associated colon tumorigenesis in mice . Science Translational Medicine DOI: 10.1126/scitranslmed.aan4116.
2. AXELSTAD M, BOBERG J, VINGGAARD A M, et al. 2013. Triclosan exposure reduces thyroxine levels in pregnant and lactating rat dams and in directly exposed off spring [J]. Food and Chemical Toxicology, 59: 534-540.
3. CHEREDNICHENKOA G, ZHANGA R, BANNISTERB R A, et al. 2012. Triclosan impairs excitation–contraction coupling and Ca2+ dynamics in striated muscle[J]. PNAS, 109(40): 1-6.
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