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Saccharin genotoxicity and carcinogenicity: a review


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In this study it was aimed to review saccharine’s genotoxicity and carcinogenicity. Saccharine is one of the most common sweeteners like aspartame, acesulfame K, and cyclamates. It is not metabolized in the gastrointestinal (GI) tract and therefore does not affect blood insulin levels. Saccharine -300 times sweeter than sucrose- is commonly used in many foods like soft drinks, baked goods, jams, canned fruit, candy, salad dressing, dessert etc. Because saccharine is consumed by millions of people, including children and even fetuses, it takes great public health significance and great of interest to the public about its safety. Too many studies have been done for the safety of saccharine. In this study, it was reviewed the all literatures between 1975 and 2014 about saccharine’s safety. According to the literatures on the genotoxicity and carcinogenicity of saccharine is still confusing. So, consumers should be careful to the consumption of this artificial sweetener.
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© by PSP Volume 37 – No 3. 2015 Advances in Food Sciences
Aslı Uçar1 and Serkan Yilmaz*2
1 Ankara University, Faculty of Health Sciences, Department of Nutrition and Dietetics, Aktaş Kavşağı Altındağ, 06340, Ankara, Turkey
2 Ankara University, Faculty of Health Sciences, Department of Midwifery, Aktaş Kavşağı Altındağ, 06340, Ankara, Turkey
In this study, it was aimed to review saccharine’s gen-
otoxicity and carcinogenicity. Saccharine is one of the
most common sweeteners like aspartame, acesulfame K,
and cyclamates. It is not metabolized in the gastrointestinal
(GI) tract and, therefore, does not affect blood insulin lev-
els. Saccharine -300 times sweeter than sucrose- is com-
monly used in many foods like soft drinks, baked goods,
jams, canned fruits, candy, salad dressings, dessert etc. Be-
cause saccharine is consumed by millions of people, in-
cluding children and even fetuses, it takes great public
health significance, and great of interest to the public about
its safety. Too many studies have been done for the safety
of saccharine. In this study, it was reviewed the all litera-
tures between 1975 and 2014 about saccharine’s safety.
According to the literature, genotoxicity and carcinogenic-
ity of saccharine is still confusing. So, consumers should
be careful to the consumption of this artificial sweetener.
Saccharine, safety, genotoxicity, carcinogenicity, nutrition
Artificial sweeteners are used as sugar substitutes in
called “zero” or “light”- beverages, foodstuffs, pharmaceu-
ticals and personnel care products [2]. They have been used
by consumers to achieve a sweet taste, for reasons of eco-
nomics, blood glucose control, or energy control [2]. The
most common sweeteners are aspartame, acesulfame K, sac-
charin, and cyclamates. The first generation of the sweetener
saccharin was produced in 1878 by Constantin Fahlberg [3].
Although saccharin was commercialized not long after its
discovery, it was not until sugar shortages during World
War I, that its use became widespread. Its popularity further
increased during the 1960s and 1970s, since saccharin is a
calorie-free sweetener [3]. Saccharin was originally listed
as GRAS. FDA proposed a ban on saccharin under the
Delaney Clause because of an association with bladder
cancer in laboratory animals in 1958 [2]. Not convinced of
saccharin's safety, because of the (inconsistent) evidence of
bladder tumors in saccharin-treated F1 male rats, the FDA
proposed a ban on its use as a food additive [4]. In 1996,
the ban was withdrawn and the zero-risk standard changed
to one of “reasonable certainty of no harm.” In 2000, sac-
charin was widely used, often in combination with other
sweeteners [2].
Saccharin (1,1-dioxo-1,2-benzothiazol-3-one) is
300 times sweeter than sucrose [5]. It is not metabolized in
the body and is heat-stable [6]. In the food industry, it is
commonly used in soft drinks, baked goods, jams, canned
fruit, candy, salad dressings, dessert toppings, and chewing
gum, in addition to being used as a tabletop sweetener. An
important characteristic of saccharin is that its sweetening
power is not reduced when heated, which makes it an ex-
cellent candidate as an additive in low-caloric and sugar-
free products. Saccharin is not metabolized in the gastroin-
testinal (GI) tract and, therefore, does not affect blood in-
sulin levels [7]. For the risk characterization of non-nutri-
tive sweeteners, the Joint Food and Agriculture Organiza-
tion/World Health Organization Expert Committee on Food
Additives (JECFA) had established an acceptable daily in-
take (ADI) of 5 mg/kg body weight for saccharin (SAC),
European Union, US FDA, Japan, France, China and Tai-
wan [8]. As per a 2010 report in Current Oncology, one
would have to drink about 800 twelve-ounce diet sodas
containing saccharin to reach doses that can induce carcin-
ogenesis [9].
Concerns with regard to the safety of saccharin are of
great public health significance and of great interest to the
public, because saccharin is consumed by tens of millions
of people, including children and even fetuses. Any evi-
dence of carcinogenesis -- and there is ample such evidence
-- of such a widely used chemical should spur health offi-
cials to minimize human exposure to it [10]
There are lots of studies about saccharin effects on
health. Some studies found that use of saccharin is associ-
ated with an increased feeling of hunger [11-13]. A rat
study showed that their diets were sweetened with saccha-
rin for over 5 weeks, presented greater weight gain and ad-
iposity, as well as a decrease in the central body tempera-
ture, when compared to glucose supplementation [14]. In
another study, it was found that when taken together, the
use of aspartame, acesulfame, cyclamate and saccharin in
© by PSP Volume 37 – No 3. 2015 Advances in Food Sciences
foods may be considered as safe, with regard to no effects
on CYP1A1 induction and activation of AhR and GR re-
ceptors [15]. A few epidemiological studies also found
some relationships between saccharin and bladder cancer
risk in humans [16-19], but most – and the largest – studies
found no association [20-22]. In this study, we aimed to
review geno-toxic and carcinogenic effects of saccharine.
This survey was conducted to gather available infor-
mation and providing an overall perspective on the geno-
toxicity and carcinogenicity of saccharin. A literature
search on genotoxicity and carcinogenicity of saccharin
was performed in the Pubmed, Scopus, Web of Science,
Science-Direct databases from year 1975 to 2014 (Octo-
ber). From the published literature, 11 genotoxicity studies
and 13 carcinogenicity studies were analyzed.
3.1 Genotoxicity
In reports of IARC [23, 24], Ashby [25], Tennant [26]
and Williams [27], saccharin was not active in in vitro
short-term and in vivo genotoxicity tests. However, it has
been found to induce SCE in human lymphocytes and plant
cells in vitro, at doses as high as 25–50 mM [28]. Jeffrey
and Williams [29] tested the geno-toxic activity of saccha-
rin in the rat hepatocyte DNA repair assay (from F344 and
Sprague-Dawley rats). Authors have reported that saccha-
rin was negative in this assay. Sasaki et al. [30] determined
the genotoxicity of sodium saccharin in male ddY mice us-
ing comet assay on the glandular stomach, colon, liver, kid-
ney, urinary bladder, lung, brain, and bone marrow, and
24 h after treatment. A hundred, 1000 and 2000 mg/kg doses
for 3-h treatment and 2000 mg/kg dose for 24-h treatment
were orally administered to male mice. Sodium saccharin
significantly increased the DNA damage in the glandular
stomach and colon. Bandyopadhyay et al. [31] evaluated
the mutagenicity of the saccharin in the Ames/Salmonella/
microsome test and their genotoxic potential by comet as-
say in the bone marrow cells of Swiss albino mice. Fifty,
100, and 200 mg/kg bw of saccharin was orally adminis-
tered. The comet parameters of DNA were increased in the
bone marrow cells due to the sweetener-induced DNA
strand breaks. However, none could act as a potential mu-
tagen in the Ames/Salmonella/microsome test. Icsel and
Yılmaz [32] reported the interactions of fish sperm DNA
(FS-DNA) with the sodium salt of sweetener saccharin,
and its copper and zinc complexes. They used UV–VIS ti-
tration, fluorometric competition, thermal denaturation,
viscosity and gel electrophoresis measurements. They have
reported that Na(sac) and its metal complexes showed a
moderate DNA binding affinity. Frenzilli et al. [33] inves-
tigated the in-vitro activity of saccharin using alkaline and
neutral comet assays in human leukocytes. Zero, 1, 5, 25
and 50 mM concentrations of saccharin were used for each
experiment. In the first experiment, no effects were ob-
served in alkaline conditions, whereas a significant in-
crease at the dose of 50 mM at pH 8 was detected. In the
second experiment, negative results were obtained under
both pH conditions. Authors have concluded that saccharin
is negative in the SGCE assay.
3.2 Carcinogenicity
There has been some controversy about the carcino-
genicity of saccharin in the past. Some feeding studies in-
dicated that saccharin at high dosage produced tumors;
however, several animal studies demonstrated no carcino-
genic effect of saccharin. Munro et al. [34] investigated the
carcinogenicity of saccharin in groups of 60 male and
60 female Charles River rats; 0, 90, 270, 810, or 2430 mg
saccharin/kg/day were administered to the animals for a pe-
riod of 26 months. Food consumption, body weight, and
clinical examinations were conducted weekly on all rats.
Four bladder tumors were found in the treated animals. The
tumors were transitional cell papillomata. However, sac-
charin administration was not accompanied by an increase
in tumor incidence, although high doses were associated
with reduced body weight in both sexes, and decreased
TABLE 1 - Sum of the genotoxicity of saccharin.
Test material Genotoxic end-point Results References
in vitro short-term and
in vivo genotoxicity tests
- IARC [23, 24], Ashby [25],
Tennant [26]and Williams [27]
Human lymphocytes Sister chromatid exchanges + Zhang et al. [28]
Plant Sister chromatid exchanges + Zhang et al. [28]
F344 and Sprague-Dawley rats Rat hepatocyte DNA repair assay - Jeffrey and Williams [29]
Male ddY mice glandular stomach, colon, liver, kidney,
urinary bladder, lung, brain, and bone mar-
row comet assay
+ (glandular stom-
ach and colon)
Sasaki et al. [30]
Salmonella typhimurium Ames - Bandyopadhyay et al. [31]
Swiss albino mice Comet assay + Bandyopadhyay et al. [31]
Fish sperm DNA DNA binding affinity +/- Icsel and Yılmaz [32]
Human leukocytes Alkaline and neutral comet assays - Frenzilli et al [33]
Footnote: + (Positive), - (Negative)
© by PSP Volume 37 – No 3. 2015 Advances in Food Sciences
TABLE 2 -Sum of the carcinogenicity of saccharin in animal models.
Test material Carcinogenicity model Results Reference
Male and female Charles River
Bladder tumors - Munro et al. [34]
Bladder tumors + Howe et al. [16]
Rats and mice Bladder tumors + Reuber [37]
Bladder tumors - Risch et al. [35]
Bladder tumors - Morgan and Wong [36]
Rats Bladder tumors + Cohen et al. [39], Zurlo and
Squire [38], Andreetta et al.
Monkey Bladder tumors - Takayama et al. [40]
Footnote: + (Positive), - (Negative)
TABLE 3 - Sum of the carcinogenicity of saccharin in epidemiological studies.
Study design Carcinogenicity model Results Reference
Human Bladder - Armstrong and Doll [41]
Human Bladder - Jensen and Kamby [42]
1953 cases and 4154 controls Colorectum - Francheschi et al. [46]
254 bladder cancer patients and
254 Controls
Bladder + Yu et al. [43]
598 cases and 1491 controls Oral cavity and pharynx - Francheschi et al. [47]
304 cases and 743 controls Oesophagus - Bosetti et al. [48]
1031 cases and 2411 controls Ovary - Bosetti et al. [49]
460 cases and 1088 controls Larynx - Bosetti et al. [50]
2569 cases and 2588 controls Female breast - Tavani et al. [51]
1294 cases and 1451 controls Prostate - Bosetti et al. [52]
767 cases and 1534 controls Renal cell - Bravi et al. [53]
51 patients and 87 controls Urinary tract + Andreatta et al. [19]
230 patients and 547 controls, stomach - Bosetti et al. [54]
326 patients and 652 controls pancreas - Bosetti et al. [54]
454 patients and 908 controls endometrium - Bosetti et al. [54]
Footnote: + (Positive), - (Negative)
longevity in male rats. Howe et al. [16] reported a signifi-
cantly increased risk for bladder cancer among saccharin
consumers. However, the work of Risch et al. [35]) and
Morgan and Wong [36] did not confirm this finding. Reu-
ber [37] reported that saccharin is carcinogenic for the uri-
nary bladder in rats and mice, and most likely is carcino-
genic in human beings. The neoplasms of the urinary blad-
der are malignant, invade and metastasize. Male rats are
more susceptible to urinary bladder carcinogenesis than fe-
male rats. Even though carcinomas of the urinary bladder
are present in rats given the higher doses of saccharin, one
was observed in a female rat given 0.5%. Experimental
studies show also that sodium saccharin induces calcium
phosphate precipitates in rat urine, which causes irritation,
hyperplasia and, ultimately, tumors [19, 38, 39]. Takayama
et al. [40] investigated the sodium saccharin (25mg/kg)
carcinogenicity on 20 monkeys, for up to 24 years. Authors
have reported that none of the animals developed bladder
cancer or urothelial proliferations.
3.3 Epidemiological works
Armstrong and Doll [41] analyzed 19709 deaths in
view of the bladder cancer mortality in the UK, between
1966 and 1972. They compared between artificial sweet-
ener users and non-users. Authors reported that there were
no significant differences between the groups. Jensen and
Kamby [42] studied the cancer mortality in people who
were born between 1941 and 1945. There was no significant
increase in bladder cancer. Yu et al. [43] conducted a case–
control study in 254 bladder cancer patients and 254 controls
in China. They reported that, compared with non-users, by
the use of saccharine for more than 19 times per year, and
for more than 15 years, significant associations were found.
Statistically significant associations were also found for
diseases related to the urinary system. Goodman et al. [44]
reported that there was no association for saccharin con-
sumption and renal cell carcinoma in 267 patients. Gallus
et al. [45] analysed artificial sweeteners (including saccha-
rin) and cancer incidence works conducted in Italy between
1991 and 2004, with 1953 colorectum cancer cases and
4154 controls {45, 46], 598 oral cavity and pharynx cancer
cases and 1491 controls [45, 47], 304 oesophagus cancer
cases and 743 controls [45, 48], 1031 ovary cancer cases
and 2411 controls [45, 49], 460 larynx cancer cases and
1088 controls [45, 50], 2569 female breast cancer cases and
2588 controls [45, 51], 1294 prostate cancer cases and
1451 controls [45, 52], and 767 renal cell carcinoma cases
and 1534 controls [45, 53]. Authors have reported that
there is no evidence about the increased risk of cancer and
saccharin consumption at several common sites in humans.
© by PSP Volume 37 – No 3. 2015 Advances in Food Sciences
Andreatta et al. [19] studied the correlation between
the urinary tract tumors (UTT) and artificial sweetener use.
51 UTT patients and 87 controls used artificial sweeteners
(including saccharin). Authors have reported that the risk
of UTT was significantly increased in long-term (10
years) artificial sweetener users, compared with none- arti-
ficial sweetener users. Bosetti et al. [54] investigated a case
control study with 230 patients, histologically confirmed
cancers of the stomach and 547 corresponding controls,
326 of the pancreas and 652 controls, and 454 of the endo-
metrium and 908 controls. The authors reported that sac-
charin consumption is not associated with the risk of cancer
of the stomach, pancreas, and endometrium.
In conclusion, according to the literature on genotoxi-
city and carcinogenity of saccharine is still confusing. So,
consumers should be careful to the consumption of this ar-
tificial sweetener.
The authors have declared no conflict of interest.
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Received: January 27, 2015
Accepted: February 24, 2015
Serkan Yilmaz
Ankara University
Faculty of Health Sciences
Department of Midwifery
Aktaş Kavşağı Altındağ
Ankara, 06340
AFS/ Vol 37/ No 3/ 2015 – pages 138 - 142
... Luo et al. [74] indicated that saccharincan causes a hazard and risk potential to aquatic organisms, which may also affect human health. Uçar and Yilmaz [75] noted that this type of artificial sweetener may be a weak carcinogen, causing cancer of the urinary tract of male rats. Other studies have proved that saccharin can induce liver inflammation in mice [76] or could be one of the main factors causing paediatric inflammatory bowel disease [77].Studies conducted on the assessment of the possibility of saccharin and other artificial sweeteners decomposition in the chlorination process have shown that most of those compounds were persistent and not transformed by the action of reactive chlorine radicals [78].This may be related toa lack of electron-rich sites for oxidation in the compound molecule [79]. ...
Full-text available
Widespread use and the continuous increase in consumption has intensified the presence of food additives and their metabolites in the environment. The growing awareness that newly identified compounds in the environment may cause a real threat, both to the environment and to future generations due to the transformation they undergo in ecosystems, makes this topic a leading problem of engineering and environmental protection. This manuscript highlights the relevance of finding these compounds in water. The exposure routes and the threat, both to human health and to the aquatic environment, have been discussed. The research presented in the article was aimed at determining the degree of contamination of swimming pools with food additives. Thirteen food additives have been identified in ten tested pools. The most frequently found were antioxidants (E320, E321) and preservatives (E211, E210), which were present in all of the tested swimming pools, both public and in private backyards. Ascorbic acid (E300) and citric acid (E330) occurred in all of the tested private swimming pools, while aspartame (E951, sweetener) and canthaxanthin (E161g, colour) were identified only in private pools. The hazard statements according to the European Chemicals Agency indicate that the identified compounds may cause both immediate effects (skin or eye irritation, allergic reactions) and also long-lasting effects, e.g., damaged fertility or genetic defects.
... 1,2-benzisothiazol-3(2H)-one 1,1-dioxide (C 7 H 5 NO 3 S), well-known as saccharin, is one of the most popular artificial sweeteners and millions of people consume it through several foods and beverages, especially calorie-free drinks (Pang et al., 2020;Uçar and Yilmaz, 2015). It is also widely used in pharmaceutical and personal care products, preservatives, adhesive removal, etc. ...
Persistent and mobile chemicals (PMs) and per- and polyfluoroalkyl substances (PFAS) are groups of chemicals that have received recent global attention due to their potential health effects on the environment and humans. In this study, exposure to a broad range of PMs and PFAS was investigated in Flemish adolescents’ urine samples (n = 83) using a suspect screening approach. For this purpose, three sample preparation methods were evaluated, and a basic liquid-liquid extraction was optimized for urine analysis based on the extraction efficiency of PMs (53–80%) and PFAS (>70%). In total, 9 PMs were identified in urine samples at confidence levels (CL) 1–3 and, among them, acetaminophen, 4-aminophenol, 2,2,6,6-tetramethyl-4-piperidone, trifluoroacetic acid (TFAA), sulisobenzone, ethyl sulfate, and 1,2-benzisothiazol-3(2H)-one 1,1-dioxide were confirmed at CL 1 and 2. In addition, the detection and identification of 2,2,6,6-tetramethyl-4-piperidone, 4-aminophenol, TFAA, and m-(2,3-epoxypropoxy)-N,N-bis(2,3-epoxypropyl) aniline (CL 3), has been reported for the first time in human urine in this study. For PFAS, only 2 compounds were identified at CL 4, implying that urine is not a suitable matrix for suspect screening of such compounds. A significant difference between sexes was observed in the detection rate of identified PMs, in particular for acetaminophen, 4-aminophenol, and sulisobenzone. The findings of this study can be used in future human biomonitoring programs, such as by including the newly identified compounds in quantitative methods or monitoring in other human matrices (e.g., serum).
... But, consumers should be careful to the consumption of artificial sweetener such as saccharin. 6 Saccharin's coordination chemistry is very vital and important in both medicinal chemistry and inorganic synthesis. Despite the fact that there is no metal complexes with saccharine molecule itself, the saccharinate anion [sac 1 = 4 (C7H4NO3S))] acts as multifunctional ligand and it can forms a lot of complexes with many metal ions easily because of the presence of the negative charged Nitrogen, the two sulfonyl oxygen and the carbonyl oxygen atom. ...
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A Jahn-Teller distorted octahedral cobalt(II) complex with saccharin and water ligands was synthesized and characterized using single-crystal X-ray diffraction, density functional theory calculation, surface analysis (MEP and Hirshfeld) and molecular docking studies. Co(II) center is six-coordinated in a distorted octahedral arrangement, with the two water O atoms located in the axial positions, and the two water O atoms and the saccharin N atoms located in the equatorial plane. Theoretical molecular modeling was carried out with Density Functional Theory (DFT) using UB3LYP with hybrid function LANL2DZ. To support intra-molecular and inter-molecular bondings in crystal structure, molecular electrostatic potential (MEP) and Hirshfeld surfaces are generated and visualized. The molecular docking analysis was investigated between cobalt complex ligand and the receptor of breast cancer mutant PDB: 3HB5-oxidoreductase.
... Remsen et Fahlberg. Elle n'est pas absorbée dans le tractus gastro-intestinal et n'affecte donc pas la glycémie ou la sécrétion d'insuline(Yilmaz and Uçar, 2015). La saccharine a un goût amer et métallique et possède un pouvoir sucrant 300 fois plus élevé que le saccharose. ...
Les glucides et les édulcorants sont détectés par des récepteurs du goût sucré à la membrane apicale des cellules entéroendocrines (CEE). Ces récepteurs hétérodimères T1R2-T1R3 sont couplés à la protéine G gustducine dont la sous-unité α est codée par le gène GNAT3. L’activation de ces récepteurs entraine une cascade de signalisation conduisant à la sécrétion de GLP-1 par les CEE. Les maladies métaboliques sont associées à des altérations de l’homéostasie glucidique et énergétique. Elles entrainent une diminution de la concentration plasmatique en GLP-1, dont la sécrétion est restaurée après rémission. L’objectif de ma thèse a été d’étudier le rôle de la voie de transduction du goût sucré, et de l’α-gustducine, dans les maladies métaboliques et leur rémission. Les résultats obtenus dans l’intestin montrent que cette voie de signalisation est exprimée spécifiquement dans les CEE. De plus, l’obésité conduit à une altération de cette voie dans les CEE et notamment à une sous-expression de GNAT3 participant au défaut de sécrétion du GLP-1. Dans l’amélioration métabolique après remodelage intestinal, la restauration de la sécrétion de GLP-1 est en partie due à une sur-expression de GNAT3 dans l’anse alimentaire. En revanche, le microbiote intestinal dysbiotique n’a pas d’impact significatif sur l’expression de GNAT3 dans l’obésité. Pour conclure, cette étude montre le rôle de la voie de transduction du goût sucré dans le défaut de sécrétion de GLP-1 dans les maladies métaboliques. L’identification de molécules pouvant stimuler la voie intestinale de transduction du goût sucré permettrait de stimuler la sécrétion endogène de GLP-1 chez les patients obèses avec ou sans diabète.
... Previously thought to be linked to bladder cancer, sodium saccharin was listed as a potential carcinogen, but because of lack of consistent evidence, it has been delisted (Uçar and Yilmaz, 2015). Sodium lauryl sul-phate is a synthetic detergent and antibacterial agent that is used to lower the surface tension and loosen the food debris and contaminants, thereby making it easier to rinse them out along with the foam generated. ...
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Antimicrobial chemotherapeutic agents have been recommended for lowering oral bacteria growth. The main purpose of this study is to examine the efficacy of different toothpaste formulations in providing complete oral cavity protection against oral pathogens. By using a modified well agar diffusion assay, twenty kinds of toothpaste were examined for antimicrobial efficacy against two oral pathogens: Streptococcus aureus and Escherichia coli. The examination indicated that the majority of the non-herbal dentifrices and combinations of herbal and chemical-based dentifrices chosen for the investigation were viable against both microbial strains, however, to differing degrees. TP1 and TP17 were found the best against E. coli and S. aureus, respectively, with 21.553 mm and 23.443 mm as the zone of inhibition. From the herbal dentifrices, TP15 was found to have significant effect on E. coli, followed by TP19 for S. aureus. Nevertheless, toothpaste TP15 and TP19 were not effective against S. aureus and E. coli, respectively. In correlation, the inhibition zones of every single other dentifrice were found to be less. Antimicrobial activity against test organisms was stronger in a sodium lauryl sulphate-based dental formulations, when combined with fluoride. A formulation including TP15 exhibited substantial activity against the tested bacterium E. coli among herbal dentifrices. Statistical analysis demonstrated that the effectiveness against Gram-negative bacteria was greater than against Gram-positive bacteria. Furthermore, herbal toothpaste can be incorporated with chemotherapeutic agents to enhance its effectiveness against pathogens present in the oral microbiome. This comparison aids in the identification of the toothpaste’s shortcomings and benefits over other formulations, widening the scope of more potent toothpaste products.
... Berdasarkan hasil penelitian yang dilakukan Ucar & Yilmaz pada tahun 2015, natrium sakarin bersifat karsinogenik dan menyebabkan kematian pada tikus (Uçar & Yilmaz, 2015). Hal ini sejalan dengan hasil penelitian Das Neves, dkk pada tahun 2010 yang menunjukkan bahwa penggunaan pemanis buatan sakarin dapat menyebabkan tumor ginjal pada tikus, dan berpotensi menyebabkan kanker pada manusia (Das Neves dkk., 2020) ...
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Zat pemanis ini merupakan suatu senyawa yang secara sengaja ditambahkan dan digunakan untuk meningkatkan cita rasa dan aroma, memperbaiki sifat-sifat fisik, sebagai pegawet, memperbaiki sifat-sifat kimia dan sumber kalori bagi tubuh. Zat pemanis ada dua jenis yaitu pemanis alami dan pemanis buatan. Produsen minuman dan pangan seperti produsen bubble drink lebih memilih untuk menggunakan pemanis buatan dibandingkan pemanis alami karena harga lebih murah dan tingkat kemanisan pemanis buatan lebih tinggi dibandingkan pemanis alami. Pemanis buatan seperti sakarin dan siklamat jika dikonsumsi secara berlebih dapat memicu terjadinya gangguan kesehatan seperti penyakit saraf, hipertensi, dan kanker otak.Jenis penelitian adalah ekperimental dengan purposive sampling. 25 sampel diperoleh dari penjual bubble drink yang berada di 5 kecamatan yang dijual di kota Surakarta. Tempat penelitian dilaksanakan di Laboratorium Kimia STIKES Nasional. Uji kualitatif yang digunakan menggunakan rapid test kit sakarin dan siklamat. Hasil uji kualitatif pada 25 sampel menggunakan rapid test kit menunjukkkan hasil negatif, tidak ditemukan adanya pemanis sakarin dan siklamat.
... Существуют серьезные опасения в отношении безопасности сахарина, поскольку его потребляют миллионы людей, включая детей. Согласно исследованиям, генотоксичность и канцерогенность сахарина вполне возможна и следует соблюдать осторожность в отношении его потребления [39]. ...
Conference Paper
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В статье рассматривается проблема влияния факторов внешней среды, окружающих человека с риском возникновением онкологических заболеваний. Рассматривается канцерогенное воздействие таких токсических факторов как курение, алкоголь, профессиональные вредности, канцерогены, содержащиеся в воде, воздухе, почве, продуктах питания, пищевых добавках, степень их влияния на возникновение различных видов онкологической патологии.
Susu kedelai merupakan salah satu produk minuman ringan dari bahan baku kacang kedelai yang banyak dikonsumsi oleh masyarakat dikarenakan kandungan gizinya sebagai sumber protein. Dalam produksi susu kedelai terkadang ada beberapa produsen yang sengaja menambahkan Bahan Tambahan Makanan (BTM) yang berbahaya dan memiliki dampak yang buruk bagi kesehatan konsumen. Sakarin adalah zat pemanis buatan dengan rumus kimia (C7H5NO3S) berbentuk bubuk kritsal putih mudah larut dalam air, tidak berbau, dan sangat manis. Efek samping penggunaan sakarin dapat menyebabkan gangguan kesehatan jika dikonsumsi dalam waktu yang lama seperti sakit kepala, kehilangan daya ingat, hipertensi, diare, asma, dan kanker otak. Penelitian ini bertujuan untuk menentukan kadar sakarin dengan teknik pengambilan sampel secara simple random sampling menggunakan 5 sampel. Berdasarkan hasil penelitian dengan uji kualitatif dengan menggunakan metode resolsinol diperoleh 2 sampel negatif dan 3 sampel positif yang menunjukkan warna flouresensi hijau kekuningan. Selanjutnya uji kuantitatif menggunakan metode titrimetri jenis alkalimetri diperoleh kadar sampel 2 sebesar 4,4963 mg/kg, sampel 3 sebesar 2,9973 mg/kg, dan sampel 4 sebesar 3,9253 mg/kg. Dengan demikian dapat disimpulkan bahwa susu kedelai yang diperjualbelikan di supermarket kota Makassar masih aman untuk dikonsumsi karena tidak melebihi ambang batas yang telah ditetapkan Menurut PermenkI No. 033/Menkes/2012 tentang bahan tambahan makanan dengan batas maksimum sakarin yaitu 50-300 mg/kg bahan.
Saccharin (1,2‐benzisothiazol‐3(2H)‐one‐1,1‐dioxide) is the oldest artificial sugar substitute, first synthetized by Remsen and Fahlberg in 1879. One of the major advantages of the use of saccharin and its derivatives, comes from the thermal and photostability of the benzisothiazole ring. This chapter focuses on the synthesis of a selected library of molecules derived from saccharin and their application in key fields, such as ionic liquids, coordination chemistry and catalysis, and therapeutic chemistry. Saccharin can directly react through its carbonyl oxygen with electrophilic reagents. Functionalization of the sulfoxide group is possible through intramolecular reactions, by replacing the sulfonyl oxygen either by an imino or an amino nitrogen. Saccharin and its derivatives are well‐known scaffolds in scientific research, possessing very interesting results concerning their biological activity. Metal complexes of saccharin have been reported for biological activities in vitro like Carbonic Anhydrase inhibition, anticancer, and antibacterial activity.
Saccharin (SAC) is an emerging contaminant, widely detected in the environment, with potential ecotoxicity risks to aqueous organisms and human beings. Wastewater treatment plants (WWTPs) are key sources and sinks of SAC, and play a vital role in eliminating SAC entering the environment. An overview is provided of the potential ecotoxicity of SAC, its occurrence in the aqueous environment, and its degradation performance in WWTPs. SAC treatments, including physical, chemical (mainly advanced oxidation processes AOPs), biological, and hybrid processes, and possible degradation mechanisms are also considered. Of the various SAC removal processes, we find that adsorption-based physical methods exhibit relatively poor performance in terms of SAC removal, whereas chemical methods, especially hydroxy radical-mediated oxidation processes, possess excellent capacities for SAC elimination. Although biological degradation can be efficient at removing SAC, its efficiency depends on oxygen supply and the presence of other co-existing pollutants. Hybrid aerobic biodegradation processes combined with other treatments including AOPs could achieve complete SAC reduction. Furthermore, novel adsorbents, sustainable chemical methods, and bioaugmentation technologies, informed by in-depth studies of degradation mechanisms and the metabolic toxicity of intermediates, are expected further to enhance SAC removal efficiency and enable comprehensive control of SAC potential risks.
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We investigated the in vitro activity of 8 chemicals of pharmaceuticals and alimentary interest by using both the alkaline and the neutral version of the Comet assay (Single Cell Gel Electrophoresis, SCGE). Aspirin (ASA), eugenol, (EUG), paracetamol (PCM) quercitin (QRC) and saccarine (SAC) were chosen because contradictory results on their genotoxicity have been reported in literature. Beside these, four compounds known to induce a wide range of genotoxic effects were included: the aneuploigenic chemical colcemid (COLC), the DNA repair inhibitor caffeine (CAFF), and the crosslinking inducer methylglyoxal (MTGL). Bleomycin (BLM) was used as positive control. The SCG test showed a good reproducibility between replicated experiments and a good specificity. The contemporary use of the dual dye viability assay and the neutral version of the Comet assay has allowed a better evaluation of the possible mechanism of action of the tested compounds, with particular regard to cell toxicity, allowing to avoide false positive results.
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  The Food Additives Amendment of 1958 is the foundation for the U.S. food additive regulatory program, which oversees most substances added to food. This article is a comprehensive review of the program, including original analysis of pre- and postmarket safety standards for various categories and subcategories of substances and their uses; assigning the more than 10000 substances currently allowed in human food to those categories; and analyzing the U.S. Food and Drug Administration's (FDA) review of more than 1900 petitions and notifications received from 1990 to 2010. Overall, federal agencies made approximately 40% of the 6000 safety decisions allowing substances in human food. These decisions allowed an estimated 66% of the substances currently believed to be used in food. Manufacturers and a trade association made the remaining decisions without FDA review by concluding that the substances were generally recognized as safe (GRAS). Robust premarket safety decisions are critical since FDA has limited resources to monitor potentially significant scientific developments and changing uses of a substance after it enters commerce and only has access to published data or data submitted to it. In the late 1990s, FDA moved from promulgating rules for its decisions for food contact and GRAS substances to reviewing manufacturer safety decisions and posting the results of the review on the agency's website. This shift appears to have encouraged manufacturers to submit their decisions to FDA for review but has limited public opportunity to provide input.
In this present work authors undertook an investigation on glucose, artificial sweetener and saccharin. This study compared the reality of the claimed sugar free nature of commercial artificial sweetener. A molecular level investigation is carried out by using FTIR spectroscopy and optical polarization experiment. The result obtained show that the sugar content of the artificial sweetener is substantial.
The interactions of fish sperm DNA (FS-DNA) with the sodium salt of sweetener saccharin (sacH) and its copper and zinc complexes, namely [M(sac)2(H2O)4]·2H2O (M = CuII or ZnII) were studied by using UV-Vis titration, fluorometric competition, thermal denaturation, viscosity and gel electrophoresis measurements. The intrinsic binding constants (Kb) obtained from absorption titrations were estimated to be 2.86 (±0.06) x 104 M−1 for Na(sac), 6.67 (±0.12) x 104 M−1 for Cu-sac and 4.01 (±0.08) x 104 M−1 for Zn-sac. The Cu-sac complex binds to FS-DNA via intercalation with a KA value of 50.12 (±0.22) x 104 M−1 as evidenced by competitive binding studies with ethidium bromide. Moreover, competition experiments with Hoechst 33258 are indicative of a groove binding mode of Na(sac) and Zn-sac with binding constants of 3.13 (±0.16) x 104 M−1 and 5.25 (±0.22) x 104 M−1, respectively. The spectroscopic measurements indicate a moderate DNA binding affinity of Na(sac) and its metal complexes. The suggested binding modes are further confirmed by the thermal denaturation and viscosity measurements. In addition, Cu-sac and Zn-sac show weak ability to damage to pBR322 supercoiled plasmid DNA.
The proportion of colorectal cancer attributed to dietary habits is high, but several inconsistencies remain, especially with respect to the influence of some food groups. To further elucidate the role of dietary habits, 1,225 subjects with cancer of the colon, 728 with cancer of the rectum and 4,154 controls, hospitalized with acute non-neoplastic diseases, were interviewed between 1992 and 1996 in 6 different Italian areas. The validated food-frequency questionnaire included 79 questions on food items and recipes, categorised into 16 food groups. After allowance for non-dietary confounding factors and total energy intake, significant trends of increasing risk of colorectal cancer with increasing intake emerged for bread and cereal dishes (odds ratio [OR] in highest vs. lowest quintile = 1.7), potatoes (OR = 1.2), cakes and desserts (OR = 1.1), and refined sugar (OR = 1.4). Intakes of fish (OR = 0.7), raw and cooked vegetables (OR = 0.6 for both) and fruit other than citrus fruit (OR = 0.7) showed a negative association with risk. Consumption of eggs and meat (white, red or processed meats) seemed uninfluential. Most findings were similar for colon and rectum, but some negative associations (i.e., coffee and tea, and fish) appeared stronger for colon cancer. Our findings lead us to reconsider the role of starchy foods and refined sugar in light of recent knowledge on the digestive physiology of carbohydrates and the insulin/colon cancer hypothesis. The beneficial role of most vegetables is confirmed, with more than 20% reduction in risk of colorectal cancer from the addition of one daily serving. Int. J. Cancer 72:56–61, 1997. © 1997 Wiley-Liss Inc.
To assess the dietary correlates of cancer of the ovary, the consumption of a wide range of food groups has been investigated in a case-control study conducted between January 1992 and September 1999 in 4 Italian areas. Cases were 1,031 women with incident, histologically confirmed epithelial ovarian cancer; controls were 2,411 women admitted to the same network of hospitals as the cases for acute, non-malignant and non-gynecological conditions, unrelated to hormonal or digestive tract diseases or to long-term modifications of diet. The subjects' usual diet was investigated through a validated food frequency questionnaire including 78 foods and recipes, then grouped into 18 food groups. Odds ratios (OR), and the corresponding 95% confidence intervals (CI) were estimated using unconditional multiple logistic regression models including terms for age, study center, education, year at interview, parity, oral contraceptive use and energy intake. Significant trends of increasing risk emerged for red meat (OR = 1.53 for the highest compared with the lowest quintile of consumption), whereas inverse associations were observed for consumption of fish (OR = 0.51), raw (OR = 0.47) and cooked vegetables (OR = 0.65), and pulses (OR = 0.77). © 2001 Wiley-Liss, Inc.
It is the position of the Academy of Nutrition and Dietetics that consumers can safely enjoy a range of nutritive sweeteners and nonnutritive sweeteners (NNS) when consumed within an eating plan that is guided by current federal nutrition recommendations, such as the Dietary Guidelines for Americans and the Dietary Reference Intakes, as well as individual health goals and personal preference. A preference for sweet taste is innate and sweeteners can increase the pleasure of eating. Nutritive sweeteners contain carbohydrate and provide energy. They occur naturally in foods or may be added in food processing or by consumers before consumption. Higher intake of added sugars is associated with higher energy intake and lower diet quality, which can increase the risk for obesity, prediabetes, type 2 diabetes, and cardiovascular disease. On average, adults in the United States consume 14.6% of energy from added sugars. Polyols (also referred to as sugar alcohols) add sweetness with less energy and may reduce risk for dental caries. Foods containing polyols and/or no added sugars can, within food labeling guidelines, be labeled as sugar-free. NNS are those that sweeten with minimal or no carbohydrate or energy. They are regulated by the Food and Drug Administration as food additives or generally recognized as safe. The Food and Drug Administration approval process includes determination of probable intake, cumulative effect from all uses, and toxicology studies in animals. Seven NNS are approved for use in the United States: acesulfame K, aspartame, luo han guo fruit extract, neotame, saccharin, stevia, and sucralose. They have different functional properties that may affect perceived taste or use in different food applications. All NNS approved for use in the United States are determined to be safe.