Thioproline

Other Names

(4R)-1,3-Thiazolidin-3-ium-4-carboxylate(4R)-1,3-Thiazolidin-4-carbonsäure(4R)-1,3-Thiazolidine-4-carboxylic acid(4R)-4-Thiazolidinecarboxylic acid(R)-Thiazolidine-4-carboxylic acid1,3-Thiazolidane-4-carboxylic acid1,3-Thiazolidin-3-ium-4-carboxylate1,3-Thiazolidin-4-carbonsäure1,3-Thiazolidine-4-carboxylic acid4-Carboxythiazolidine4-Thiaproline4-Thiazolidinecarboxylic acid4-Thiazolidinecarboxylic acid, (R)-4-Thiazolidinecarboxylic acid, L-Acide (4R)-1,3-thiazolidine-4-carboxyliqueAcide DL thiazolidine carboxylique-4Acide thiazolidine-4-carboxyliqueDL-ThiaprolineDL-Thiazolidine-4-carboxylic acidDL-ThioprolineGamma-thiaprolineH-Thiopro-OHH-Thz-OHL-4-Thiazolidinecarboxylic acidL-T4CL-ThiaprolineL-Thiazolidine-4-carboxylateL-Thiazolidine-4-carboxylic acidL-ThioprolineThiaprolineThiazolidine-4-carboxylic acidThiobilineThioproline zwitterionTimonacictProγ-Thioproline

Synopsis

Thioproline (L-Thiazolidine-4-Carboxylic Acid): A Comprehensive Reference

1. Identity: Chemical Names, Structure, and Natural Occurrence

1.1 Chemical Identity

Thioproline is a nonproteinogenic amino acid with the molecular formula C₄H₇NO₂S. It consists of a 1,3-thiazolidine ring substituted with a carboxylic acid. It is a cyclic sulfur amino acid — specifically, a condensation product of cysteine and formaldehyde. The full set of names used in the scientific literature includes:

IUPAC name: 1,3-thiazolidine-4-carboxylic acid
Common synonyms: Thioproline, thiazolidine-4-carboxylic acid (TC or TAC), L-thioproline, timonacic
CAS registry number: 444-27-9
Pharmaceutical trade names: Timonacic (brand names Heparegen or Arbitol) is used for the treatment of liver diseases. It is also marketed internationally under the names Heparegen and Arbitol.

Thioproline is a sulfur-containing amino acid that is proline in which the methylene group at position 4 is replaced by a sulfur atom. It has a role as a hepatoprotective agent, an antioxidant, and an antidote. It is classified as a sulfur-containing amino acid, a thiazolidinemonocarboxylic acid, and a non-proteinogenic alpha-amino acid.

1.2 Structural Relationship to Proline and Cysteine

L-Thiazolidine-4-carboxylic acid (thioproline) is recognized as a structural proline analogue. Like proline, it contains a cyclic secondary amine. It causes linear growth inhibition in E. coli, and this inhibition is specifically reversed by the simultaneous addition of L-proline.

Thioproline (TPRO) and methylthioproline (MTPRO) are the condensation products of cysteine with formaldehyde and acetaldehyde, respectively. TPRO and MTPRO are thought to be "frozen" cysteines because they liberate cysteine in the liver and protect the liver.

1.3 Natural Occurrence

It is synthesized by the reaction of formaldehyde and cysteine and occurs in nature, but rarely. This compound has been reported in Arabidopsis thaliana, Lentinula edodes (shiitake mushroom), and other organisms.

The formation of thioproline in foods is closely tied to cooking reactions between naturally present cysteine residues and formaldehyde. Thioproline has been found in various cooked foods such as cod fish, shiitake mushroom, and various kinds of cooked vegetables. More specifically, TPRO was ubiquitously found in various cooked foods, such as vegetables (~2 ppm), cod (~5 ppm), shiitake mushrooms (~10 ppm), and liver-based foods (~15 ppm).

A systematic study of Asian leguminous seeds found that amounts of thioproline in various edible leguminous seeds were determined. Thioproline in uncooked Parkia speciosa (the most popular seeds eaten in the south of Thailand) was undetectable, but increased markedly to 0.14 ± 0.02 mmol/100 g after boiling. The formation of thioproline was effectively inhibited by the addition of N-ethylmaleimide, a thiol-trapping agent. The uncooked Parkia speciosa seeds contained substantial amounts of formaldehyde and thiol compounds, and the amounts decreased after boiling, confirming that the cooking process itself drives the condensation reaction. Thioproline was also found in Djenkol beans eaten in Indonesia and in Parkia speciosa seeds and other edible leguminous beans eaten in Thailand and Malaysia.

Research on Korean fermented foods confirmed that thioproline and methylthioproline were identified and quantified in various traditional Korean fermented foods by LC–APCI–MS/MS. These foods are traditionally manufactured from meju, which is a fermented rectangular block of crushed and cooked soybeans.

1.4 Pharmaceutical and Supplement Forms

As a pharmaceutical preparation, thioproline is most commonly taken as an oral tablet. In laboratory and clinical research settings, it may be administered via intravenous (IV) injection. In the pharmaceutical and cosmetics industry, timonacic (thioproline, 1,3-thiazolidine-4-carboxylic acid, tPro) is quantified in pharmaceutical tablets and face care products including creams, sera, foundations, and suncreams.

2. Traditional and Historical Use

Thiazolidine-4-carboxylic acid (TC) is a cyclic sulfur amino acid, a condensation product of cysteine and formaldehyde. Its chemistry, biological effects, and clinical use have been formally reviewed in the scientific literature.

Thioproline does not belong to a historically documented traditional herbal or botanical materia medica — it is not a plant extract, herb, or traditional remedy in the conventional sense of, for example, Ayurvedic or Chinese medicine. Rather, its history is a 20th-century pharmaceutical one: TC has been clinically used for about 20 years (as of the 1982 review, placing the onset of clinical use in Europe to approximately the early 1960s).

Extensive animal experiments and studies on human subjects carried out in Europe indicated that a combination of TC and folic acid, known commercially as "Folcysteine," had revitalizing effects on age-related biochemical variables of blood and tissues. Further animal studies confirmed the anti-toxic effects of TC, particularly on the liver.

Thioproline was the first inducer of reverse transformation of neoplastic cells to be tested, with encouraging activity, in cancer patients. This initial application came primarily from European oncology research during the 1970s and early 1980s.

Thioproline is currently investigational in the United States and is not yet FDA-approved for standard cancer treatment. However, it is an approved prescription medication in several European countries for the management of liver diseases.

Thioproline (1,3-thiazolidine-4-carboxylic acid, timonacic, tPro) is a conjugation product of cysteine and formaldehyde, which exhibits a wide variety of health-promoting properties. In particular, tPro has attracted interest as a drug due to its antioxidant, hepatoprotective, anticancer, and immune-stimulating properties.

3. Key Constituents, Biochemistry, and Mechanisms of Action

Because thioproline is itself a single defined chemical compound rather than a botanical extract, this section describes its molecular properties and known biochemical mechanisms.

3.1 Cysteine Release and Glutathione Precursor Activity

One of the most pharmacologically significant properties of thioproline is its metabolic conversion to cysteine and its role as an indirect glutathione (GSH) precursor. TAC (thiazolidine-4-carboxylic acid) is oxidized by mitochondrial proline oxidase of the liver and kidney to L-thiazoline-(4)-carboxylic acid, which then is hydrolyzed to N-formyl-cysteine (FCYS). FCYS is hydrolyzed to cysteine and formic acid by a cytosolic enzyme.

This metabolic pathway has direct implications for glutathione replenishment. In a study of paracetamol (acetaminophen) toxicity in human hepatocytes, several metabolic precursors were examined in vitro for their ability to increase intracellular glutathione, and the results showed the following sequence: N-acetylcysteine > thioproline > cysteine > 2-oxo-4-thiazolidine carboxylic acid > methionine. Furthermore, only N-acetylcysteine, thioproline, and cysteine substantially increased glutathione levels when 1 mM paracetamol was present in the incubation medium and thus prevented its toxicity.

3.2 Nitrite Trapping (Nitrosation Inhibition)

A second, well-documented mechanism is the capacity of thioproline to intercept nitrite under acidic gastric conditions, thereby preventing the formation of carcinogenic N-nitroso compounds. Thioproline is nitrosated about 1000 times faster than proline in vitro, and NTCA (N-nitrosothiazolidine-4-carboxylic acid) is excreted into the urine without being metabolized. Thioproline has therefore been proposed as an effective nitrite-trapping agent in the human body.

N-Nitrosothiazolidine-4-carboxylic acid (NTCA; N-nitrosothioproline) is one of the predominant N-nitroso compounds in human urine; importantly, it is also nonmutagenic and, presumably, noncarcinogenic. This is a critical safety feature: unlike many N-nitroso compounds, thioproline's nitrosation product is not genotoxic, meaning that the nitrite is rendered harmless rather than converted into a dangerous form.

The gastrointestinal tract has a unique mechanism for nitric oxide (NO) capture in the form of N-nitrosamines. N-Nitrosamines are formed by the reaction between thioproline and NO under the acidic conditions prevalent in the stomach. The nitrosamines thus formed are excreted in the urine and act as an important biomarker for human NO concentrations.

3.3 Structural Analogy to Proline

Thioproline, or a closely related metabolic derivative, can be incorporated into bacterial proteins. Proline antagonizes the incorporation of thioproline into protein. The analogue specifically inhibits the rate and extent of prolyl-ribonucleic acid formation. This competition with proline is primarily of experimental and basic-science interest; at physiological doses, the relevance to human health remains undetermined.

3.4 Reverse Transformation / Antineoplastic Mechanism (Contested)

Acting on cellular membranes of malignant cells through an unknown mechanism, timonacic may induce malignant cells to revert back to an untransformed state. This agent may also restore contact inhibition, a phenomenon characterized by the paracrine inhibition of mitosis following the formation of a critical cell mass. Timonacic may also produce antioxidant effects secondary to its release of cysteine and restoration of glutathione concentrations. It should be noted, however, that this mechanism has been contested (see Section 5).

3.5 Proline Oxidase Substrate Activity and Formaldehyde Capture

The toxicity and mutagenicity of formaldehyde (HCHO) lie in its ability to react spontaneously with amino and thiol groups. With amines such as the 6-amino group of peptidyl lysine, HCHO forms a carbinolamine. With thiols, notably free and peptidyl cysteine, HCHO forms the cyclic derivative thioproline (thiazolidine-4-carboxylate). Research in bacteria has shown that HCHO is known to react spontaneously with cysteine to form the close proline analog thioproline (thiazolidine-4-carboxylate), which is incorporated into proteins. In this sense, endogenous thioproline formation represents a dual-edged biochemical event: it sequesters reactive formaldehyde, but its incorporation into proteins may itself be toxic at high formaldehyde loads.

3.6 Rotational Conformation

The broadband rotational spectrum of jet-cooled laser-ablated thioproline has been recorded in modern structural studies. This physical chemistry work has confirmed the compound's ring geometry and identified two stable rotamers, providing structural clarity relevant to its binding behavior in biological systems.

4. Scientific Evidence by Area of Use

4.1 Hepatoprotection (Liver Protection)

Preclinical evidence: Animal studies confirmed the anti-toxic effects of TC, particularly on the liver. The mechanistic basis for this is well established: thioproline liberates cysteine upon hepatic metabolism, which is a rate-limiting substrate for glutathione biosynthesis. Studies in human hepatocytes demonstrated that thioproline ranked second only to N-acetylcysteine in its ability to restore intracellular glutathione when cells were challenged with a hepatotoxic dose of paracetamol, and it substantially prevented paracetamol-induced cytotoxicity in vitro.

L-Thiazolidine-(4)-carboxylic acid (TAC) has proven to be a good substrate for long-term parenteral nutrition. This finding is relevant because cysteine itself is unstable in parenteral nutrition solutions, while thioproline, as a "protected" form of cysteine, provides greater chemical stability.

Clinical evidence and regulatory status: Timonacic (brand names Heparegen or Arbitol) is used for the treatment of liver diseases in several European countries. However, formal high-quality randomized controlled trial data evaluating hepatoprotective endpoints in human patients are limited in the publicly available English-language literature. The evidence for its liver-protective role in humans remains largely inference from mechanism and animal studies.

4.2 Nitrite Trapping and Cancer Chemoprevention

Human evidence (single-subject dose study): The nitrite trapping capacity of thioproline was evaluated in a male nonsmoking volunteer ingesting nitrate and eating a controlled diet. The highest level of NTCA excreted, 5.89 μmol, was measured after the subject ingested 6 mmol NO₃⁻ followed by 0.45 mmol (60 mg) thioproline. The effective amount of nitrite was estimated to be 0.3% of the ingested NO₃⁻; for 6 mmol NO₃⁻ ingested, the calculated effective amount of NO₂⁻ was 18 μmol, and 33% of this nitrite was trapped by ingestion of 0.45 mmol thioproline. The investigators concluded that thioproline is a sensitive probe for evaluating human nitrosating capacity and an effective nitrite-trapping agent. This was a single-subject study and therefore constitutes only weak evidence for clinical efficacy.

Animal (rodent) carcinogenesis inhibition: A controlled animal study examined thioproline's capacity to suppress nitrosation-driven carcinogenesis. Two groups of male F-344 rats were given diet containing 0.25% N-benzylmethylamine (Group I) or 0.25% N-benzylmethylamine plus thioproline (0.25% until week 17, then 0.5%; Group II). Both groups received drinking water containing sodium nitrite (0.1% until week 17, then 0.2%). The experiment continued for 717 days. Squamous cell carcinoma of the forestomach developed in six out of seven rats in Group I and in significantly fewer — two out of nine rats — in Group II. The degree of tumor invasion was also less in the thioproline-treated group. Thus thioproline suppressed carcinogenesis induced by N-benzylmethylamine and nitrite, possibly by inhibiting the in vivo nitrosation of N-benzylmethylamine.

Esophageal adenocarcinogenesis (rat model): Duodenogastroesophageal reflux causes esophageal adenocarcinoma in rats without the use of a carcinogen. This etiology may be associated with endogenous nitrosation in the gastrointestinal tract. Thioproline is an effective nitrite-trapping agent and blocks endogenous nitrosation. The effect of ingested TPRO on esophageal adenocarcinogenesis was investigated in rats with duodenogastroesophageal reflux (DGER) or gastroesophageal reflux (GER), using a series of 200 male Fischer 344 rats that received surgery to induce reflux.

Evidence strength for cancer chemoprevention: The mechanistic basis (nitrite trapping → reduction of N-nitroso compound formation) is chemically sound and supported by in vitro kinetics and animal carcinogenesis models. However, no randomized controlled trials in humans have been published demonstrating a reduction in cancer incidence from thioproline supplementation. The evidence is preliminary and based primarily on animal experiments and basic biochemistry.

4.3 Antineoplastic ("Reverse Transformation") Activity

Initial claims and clinical trials: Thioproline was the first organic inducer of reverse transformation of malignant cells in vitro that has been used as a human therapeutic with contradictory results. Thioproline was the first inducer of reverse transformation of neoplastic cells to be tested, with encouraging activity, in cancer patients. These results could not be reproduced in two subsequent clinical trials.

Laboratory pharmacology and toxicology re-evaluation: A formal pharmacologic and toxicologic evaluation (Newman et al., Cancer Treat Rep, 1980) found that the ability of thioproline to act as a nontoxic inducer of reverse transformation was examined. Thioproline was unable to effect reproducibly morphologic changes characteristic of the reversed transformed state of HeLa, WI-38VA13, C1300 neuroblastoma, and CHO-K1 cell lines. Reversal of transformed cells with dibutyryl cyclic AMP was, however, readily demonstrated in both the CHO-K1 and C1300 cell lines. Thioproline produced severe, life-threatening CNS toxicity in both mice and rats at levels far below those previously reported to be without any toxic effects.

Proposed explanation for discrepancy: The possible reason for the irreproducibility could be that, in the first active trials, the patients may have taken other non-cancer-related drugs that, by acting on the cyclic AMP and prostaglandin cascades, could have functioned as positive cooperators on the effect of thioproline. A new clinical trial, with thioproline associated with its cooperators, was proposed for tumors with no hope of improvement with cytostatics.

Genotoxicity: An in vitro genotoxicity study investigated whether thioproline induces sister chromatid exchanges (SCE) as a marker of DNA damage. Thioproline is the first organic inducer of reverse transformation of malignant cells in vitro that has been used as a human therapeutic with contradictory results. This compound does not increase SCE, but does depress PHA-induced lymphocytes mitogenesis at approximately the same concentration reported to induce restoration of contact inhibition of HeLa cells. This gives further argument to the definition of thioproline as a reverse inducer.

Evidence strength: The antineoplastic "reverse transformation" hypothesis is currently considered unproven, with reproducibility failures in formal clinical trials. The anticancer interest in thioproline as of the current literature relates primarily to its nitrosamine-blocking capacity rather than to direct anti-tumor cytotoxic or cytostatic activity.

4.4 Aging, Longevity, and Neurological Function

Animal lifespan studies: Male mice on a diet supplemented with thioproline at 2.0 g/kg of food from 28 weeks of age and for their entire life showed a 23–29% increased median and maximal lifespan. These survival increases were associated with improved neurological functions. Compared to control mice, thioproline-supplemented mice had a 20% lower integral spontaneous food intake and 10% lower body weight at 100 weeks of age. Body weight showed a statistically significant inverse relationship with survival and neurological performances.

Thioproline-supplemented mice exhibited a 58–70% decrease of the age-dependent oxidative damage in brain and liver mitochondria at 52 weeks (old mice) and 78 weeks (senescent mice) of age, respectively.

Importantly, a notable mechanistic nuance emerged from this work: in vitro, thioproline neither exhibited direct antioxidant activity nor had any effect on the electron transfer or mtNOS functional activities of brain and liver mitochondria. It is surmised that thioproline induces an anorexic effect associated with improved survival and neurological function through a decreased oxidative damage and regulation that may involve hypothalamic appetite centers. This indicates that the longevity benefit observed in mice may be mediated indirectly — potentially through reduced caloric intake — rather than through direct antioxidant action on mitochondria.

Related evidence from invertebrate models found that oral administration of hydrophilic substances such as ascorbic acid, N-acetyl cysteine, GSH, and thioproline using liposomes prolonged the lifespan of nematodes, whereas the conventional method of delivery showed no longevity effects. This delivery-route dependency highlights the importance of bioavailability.

Evidence strength: Evidence for lifespan extension is limited to animal models (mice, nematodes). No human longevity or neurological function clinical trials with thioproline have been published.

4.5 Immune Function and Aging

Animal evidence: Diet supplementation with thioproline (thiazolidine-4-carboxylic acid), an intracellular sulfhydryl antioxidant and free radical scavenger, may slow the aging process of metazoans and prolong their lifespan. In the relevant experiment, Swiss mice fed thioproline (0.07%, w/w) from 13 to 22 months of age were used, with 6- and 22-month-old mice fed standard diet as controls.

The results showed a decrease in mobility, chemotaxis, and lymphoproliferative response in old mice compared to adults. However, a significant increase in these functions was observed in old mice fed thioproline. The potential advantage of using this antioxidant for immunostimulation during aging — a stage of life characterized by a decreased immune response — was discussed.

Another study cited that thioproline administered in the diet stimulates lymphocyte and natural killer (NK) functions in old mice, as well as macrophage functions in vitro. Thioproline administered in the diet stimulates the lymphocyte and natural killer (NK) functions in old mice as well as the macrophage functions in vitro.

Evidence strength: Immune stimulation data are entirely from animal models, primarily aged mice. No human data are available for this indication.

4.6 Parenteral Nutrition: Cysteine Delivery

One of the most clinically validated applications of thioproline is as a stable cysteine source for parenteral nutrition. Free cysteine is chemically unstable and undergoes rapid oxidation in solution, limiting its use as a component of intravenous amino acid preparations. L-Thiazolidine-(4)-carboxylic acid (TAC) has proven to be a good substrate for long-term parenteral nutrition. Once infused, it undergoes hepatic metabolism to release cysteine (and formate), thus meeting the patient's cysteine requirements without the instability problems of free cysteine. The evidence for this metabolic utility is well established in biochemical and animal studies.

5. Body Systems and Health Areas Associated with Thioproline

Hepatic / Liver system: Hepatoprotective effects via glutathione replenishment; approved as a liver-disease medicine in some European countries.
Gastrointestinal system: Nitrite trapping under gastric acidic conditions; suppression of endogenous N-nitroso compound formation; potential role in esophageal cancer prevention in reflux models.
Immune system: Animal evidence for restoration of lymphocyte proliferation, NK-cell activity, and macrophage function in aged animals.
Central nervous system: Preservation of mitochondrial enzyme activities (NADH-dehydrogenase, cytochrome c oxidase, mtNOS) in aged mouse brains; timonacic (thioproline) is CNS active in animals. No human data are available.
Oncology: Nitrosation inhibition (established in animals and mechanistically in humans); reverse transformation (contested — not reproduced in clinical trials).
Nutritional biochemistry / amino acid metabolism: Cysteine carrier and glutathione precursor in clinical parenteral nutrition settings.

6. Dosage Forms and Reported Dosages

The following dosages reflect those specifically stated in the cited scientific literature, not recommendations:

Nitrite-trapping human study (single subject): 60 mg (0.45 mmol) thioproline administered orally following ingestion of 6 mmol nitrate in a controlled diet study.
Rodent carcinogenesis inhibition: 0.25% thioproline in diet (until week 17), then 0.5%, in rats also given 0.1% then 0.2% sodium nitrite in drinking water.
Mouse lifespan study: 2.0 g/kg of food, administered from 28 weeks of age for the entire life of the animals.
Mouse immune function study: 0.07% (w/w) in standard diet, fed from 13 to 22 months of age.
Pharmaceutical tablets (European market): Timonacic is quantified in pharmaceutical tablets at concentrations determined by HPLC-UV analysis; no specific daily tablet dose was extractable from the publicly available sources reviewed here.
Parenteral nutrition: TAC has been validated as a substrate for long-term parenteral nutrition, though exact clinical dosing protocols were not available in the sources retrieved.

7. Safety Considerations and Interactions

7.1 Established CNS Toxicity at High Doses (Rodent Data)

Thioproline produced severe, life-threatening CNS toxicity in both mice and rats at levels far below those previously reported to be without any toxic effects. This finding, from the formal pharmacological evaluation by Newman et al. (1980), was a critical result that contributed to the suspension of early clinical development in the United States and underscores that the therapeutic window requires careful characterization.

7.2 Regulatory Status

Timonacic (thioproline) is an investigational agent in the United States and is not currently approved by the US Food and Drug Administration (FDA) for general clinical use in cancer care or hepatology. It may be available only through participation in approved clinical trials or by prescription in specific international medical markets.

7.3 HIV Investigational Use

Timonacic has been used in trials studying the treatment of HIV Infections, though no outcome data from these trials were available in the sources consulted.

7.4 Lymphocyte Suppression

Thioproline does not increase sister chromatid exchanges (a marker of DNA damage), but does depress PHA-induced lymphocytes mitogenesis at approximately the same concentration reported to induce restoration of contact inhibition of HeLa cells. This suppression of mitogen-driven lymphocyte proliferation is an in vitro observation with uncertain clinical significance but warrants noting in the context of immune modulation.

7.5 Formation as a Driver of Formaldehyde Toxicity

Research in bacteria has illuminated a context in which thioproline formation is itself a toxicological event rather than a protective one. Certain thioproline-containing peptides are toxic, and the enzyme PepP cleaves these aberrant peptides. PepP cleaved the model peptide Ala-thioproline-Ala as efficiently as Ala-Pro-Ala in vitro and in vivo, and deleting PepP increased sensitivity to supplied thioproline. These data provide biochemical genetic evidence that thioproline formation contributes substantially to formaldehyde toxicity. This context is distinct from dietary supplementation: it applies to high-formaldehyde environments (such as engineered methylotrophic metabolic pathways in bacteria) rather than to normal physiological concentrations in humans.

7.6 Cosmetic Use Claims — Limited Evidence

In recent years, tPro has also gained interest in the cosmetics industry. As claimed by cosmetics manufacturers, tPro has anti-acne, anti-psoriatic, and anti-aging properties as well as improving structure and stimulating the growth and regeneration of the epidermis; however, this information is not supported by the literature.

7.7 N-Nitrosothioproline: Non-Mutagenic Metabolite

A specific safety consideration relevant to dietary thioproline consumption is the formation of its nitrosation product. N-nitrosothioproline (NTPRO) has been identified as a major N-nitroso compound in human urine. NTPRO is a nonmutagenic NOC, and thus is probably noncarcinogenic, like N-nitrosoproline. NTPRO is excreted into urine without further metabolic change and has been used as a sensitive monitoring probe for endogenous formation of N-nitroso compounds. This is considered a favorable safety feature: the nitrosation product is non-genotoxic and is cleared renally.

7.8 Limits of Anti-Nitrosamine Protection

While thioproline traps nitrite efficiently, its protective capacity against pre-formed, metabolically activated N-nitroso compounds is limited. Thioproline, an effective nitrite trapping agent in vivo, was examined for its detoxifying ability in rats against N-nitrosodimethylamine (NDMA) and N-nitrosocimetidine (NCIM). When NDMA (37–101.5 mg/kg) was administered with TPRO (532 mg/kg), no influence of TPRO on NDMA-induced lethality and histological results in the liver was observed. NDMA oxygenase activity measured by formaldehyde formation was not affected either. This indicates that thioproline intercepts reactive nitrosating species before they form a carcinogen, but cannot detoxify already-formed, metabolically-activated nitrosamines such as NDMA.

References

Health Conditions

Health conditions that Thioproline may help support.

No conditions available.

Body Systems

Body systems that Thioproline may help support.

No body systems available.