Schisandra for Liver Protection

Table of Contents

1. The Schisandrin Lignan Family — A, B, C, and Beyond
2. Hepatoprotection Mechanism: Glutathione, Nrf2, and Mitochondrial Stabilization
3. Animal Toxic-Liver-Injury Models (CCl4, Acetaminophen, Ethanol, Galactosamine)
4. Chinese Randomized Controlled Trial Data in Chronic Viral Hepatitis B and C
5. Bifendate (DDB) — The Synthetic Schisandrin C Derivative as a Chinese Pharmaceutical
6. Cytochrome P450 3A4 and Drug Interactions
7. Drug-Induced Liver Injury and Hepatotoxin Co-Exposure
8. Non-Alcoholic Fatty Liver Disease (NAFLD / MAFLD) Evidence
9. Practical Dosing Protocols and Standardization
10. Cautions and Contraindications
11. Key Research Papers
12. Connections
13. Featured Videos

The Schisandrin Lignan Family — A, B, C, and Beyond

The active pharmacology of Schisandra chinensis is concentrated almost entirely in its lignan content. Lignans are a structurally diverse class of plant secondary metabolites built from two phenylpropanoid units; the Schisandra lignans share a distinctive dibenzocyclooctadiene scaffold that distinguishes them from the more widely distributed lignans of flax (secoisolariciresinol), sesame (sesamin), and pine knot (pinoresinol). Roughly forty individual Schisandra lignans have been isolated and characterized since the first chemical work in the 1960s, with the principal subgroups including:

• Schisandrins — the original lignans isolated by Soviet chemists, named alphabetically: schisandrin (A), gamma-schisandrin (B), and deoxyschisandrin variants. Schisandrin A is the most abundant in the dried fruit; schisandrin B has the most potent hepatoprotective activity.
• Gomisins — a numbered series (gomisin A through gomisin Q, with letters skipped for compounds that turned out to be duplicates) characterized largely by Japanese groups in the 1970s and 1980s. Gomisin N is a particularly active hepatoprotective compound.
• Schisantherins — schisantherin A (formerly gomisin C) and its analogs, characterized by an additional ester group on the dibenzocyclooctadiene scaffold.
• Wuweizisus — named for the Chinese name wu wei zi, including wuweizisu A (a synonym for schisandrin), wuweizisu B (schisandrin B), and wuweizisu C (schisandrin C).

Within this large family, schisandrin B is the most studied single molecule. It is approximately ten-fold more potent than schisandrin A on hepatocyte glutathione induction, and the great majority of mechanism-of-action research in the past two decades has used purified schisandrin B as the molecular probe. For more on related botanicals used in liver support, see Milk Thistle, which works through a different lignan family (silymarin, including silybin A and B).

Back to Table of Contents

Hepatoprotection Mechanism: Glutathione, Nrf2, and Mitochondrial Stabilization

The molecular mechanism of Schisandra hepatoprotection has been worked out in considerable detail over four decades. The three core elements are glutathione replenishment, Nrf2 antioxidant-response activation, and direct mitochondrial-membrane stabilization.

Glutathione replenishment — Schisandrin B activates the rate-limiting enzymes of glutathione synthesis, gamma-glutamylcysteine ligase catalytic subunit (GCLC) and modifier subunit (GCLM), increasing both the synthesis rate and the steady-state concentration of glutathione (reduced glutathione, GSH) in hepatocytes. Glutathione is the dominant intracellular antioxidant and the substrate for glutathione-S-transferase-mediated phase II conjugation of toxic metabolites. Studies in cultured hepatocytes consistently show 30-60% elevations of intracellular reduced glutathione after schisandrin B exposure at clinically relevant concentrations.

Nrf2 activation — The mechanism upstream of GCLC/GCLM induction is activation of the Kelch-like ECH-associated protein 1 (Keap1) / nuclear factor erythroid 2-related factor 2 (Nrf2) signaling axis. Under unstressed conditions, Nrf2 is sequestered in the cytoplasm by Keap1 and continuously targeted for proteasomal degradation. Schisandrin B modifies redox-sensitive cysteine residues on Keap1, releasing Nrf2 to translocate to the nucleus, where it heterodimerizes with small Maf proteins and binds antioxidant response elements (AREs) in the promoter regions of more than 200 cytoprotective genes — including glutathione synthesis enzymes, glutathione-S-transferase isoforms, nicotinamide adenine dinucleotide (NAD)(P)H quinone oxidoreductase 1 (NQO1), heme oxygenase-1 (HO-1), and thioredoxin. This single transcriptional switch coordinates a broad cytoprotective response.

Mitochondrial-membrane stabilization — A third, distinct mechanism is direct stabilization of the mitochondrial inner membrane and prevention of the mitochondrial permeability transition (MPT) under oxidative or calcium-overload stress. Chiu and colleagues at the Hong Kong University of Science and Technology have published a long series of papers documenting that schisandrin B reduces mitochondrial swelling and cytochrome c release in response to pro-apoptotic stimuli, preserving adenosine triphosphate (ATP) production and preventing the apoptotic cascade in hepatocytes facing toxic insult.

Together these three mechanisms produce a cell that is more resistant to oxidative, electrophilic, and apoptotic injury — the molecular basis for the consistent hepatoprotective effects seen in animal models and the clinical reduction in transaminases seen in human chronic liver disease.

Back to Table of Contents

Animal Toxic-Liver-Injury Models (CCl4, Acetaminophen, Ethanol, Galactosamine)

The preclinical evidence for Schisandra hepatoprotection is one of the most extensively replicated bodies of botanical research in any species. The four standard toxic-liver-injury models in laboratory rodents have all been used to characterize Schisandra protection.

Carbon tetrachloride (CCl4) model — CCl4 is metabolized by cytochrome P450 2E1 (CYP2E1) to the trichloromethyl free radical (CCl3·), which lipid-peroxidates hepatocyte membranes and produces centrilobular necrosis within 24 hours. Schisandra extract or purified schisandrin B given for 3-7 days before CCl4 challenge reduces the resulting alanine aminotransferase/aspartate aminotransferase elevation by 50-80% depending on dose and reduces histological necrosis to a similar degree. Pre-treatment is required — post-injury rescue is much less effective — consistent with the upregulation-of-defenses mechanism rather than a direct antagonist effect.

Acetaminophen (paracetamol) model — Acetaminophen at toxic doses is metabolized by cytochrome P450 2E1 (and to a lesser extent CYP1A2, CYP3A4) to the reactive intermediate N-acetyl-p-benzoquinone imine (NAPQI), which depletes glutathione and forms protein adducts with hepatocyte cysteine residues. Schisandrin B pre-treatment provides substantial protection against acetaminophen hepatotoxicity in mice, with reduced alanine aminotransferase elevation, reduced glutathione depletion, and reduced histological necrosis. The mechanism is the same glutathione-replenishment pathway that N-acetylcysteine (NAC) targets clinically — the standard antidote for acetaminophen overdose.

Ethanol model — Chronic ethanol feeding in rats produces steatosis, oxidative stress, and elevated transaminases. Schisandra extract reduces ethanol-induced steatosis, normalizes alanine aminotransferase/aspartate aminotransferase, and restores mitochondrial function in the Lieber-DeCarli rat ethanol model. Mechanism includes reduction of cytochrome P450 2E1 induction (an unusual finding given that Schisandra lignans induce cytochrome P450 enzymes in other rodent studies — the CYP isoforms are differentially regulated) and restoration of mitochondrial complex IV activity.

Galactosamine model — D-galactosamine produces hepatic injury through depletion of uridine nucleotides required for RNA synthesis, producing apoptotic and necrotic hepatocyte death. Schisandrin B protects against galactosamine hepatotoxicity through preservation of mitochondrial integrity and prevention of the MPT.

The consistency of protection across four mechanistically distinct toxic-liver models — oxidative radical injury, electrophilic adduct injury, lipid-peroxidative chronic injury, and uridine-depletion injury — argues strongly that the protective mechanism is a non-specific upregulation of hepatocyte defenses rather than antagonism of any single toxic species.

Back to Table of Contents

Chinese Randomized Controlled Trial Data in Chronic Viral Hepatitis B and C

Schisandra has been used in mainland Chinese clinical hepatology for treatment of chronic viral hepatitis B and C since the 1960s. The published clinical trial base — while much of it is in Chinese-language journals not always indexed by Western databases — documents consistent reduction of serum transaminases (alanine aminotransferase and aspartate aminotransferase) in patients with chronic hepatitis, typically 60-80% normalization of elevated alanine aminotransferase within 4-8 weeks of treatment.

This Chinese clinical use was the empirical basis for the subsequent development of the synthetic analog bifendate (DDB) as a registered pharmaceutical, discussed in the next section.

Importantly, the Schisandra effect in chronic viral hepatitis is a hepatoprotective and biochemical effect — it reduces hepatocyte injury and consequently reduces transaminase release — not a direct antiviral effect. HBV DNA and HCV RNA levels are not consistently reduced by Schisandra, so it is not an antiviral treatment; the antiviral drugs are nucleoside/nucleotide analogues such as tenofovir or entecavir for hepatitis B virus (HBV) and sofosbuvir-based direct-acting antiviral regimens for hepatitis C virus (HCV). It functions as an adjunct that reduces hepatocellular damage during ongoing viral replication, with the goal of slowing progression to fibrosis and cirrhosis.

Western clinical trial evidence is comparatively sparse. The Chinese trial base remains the dominant evidence base, and the translation of those trials into Western practice has been limited by methodological heterogeneity, predominantly Chinese-language publication, and the regulatory non-pharmaceutical status of Schisandra extracts in the United States and Europe. The recent (2015-2024) literature includes a growing number of higher-quality Chinese trials in MAFLD/NAFLD with bilingual abstracts and improved methodology.

Back to Table of Contents

Bifendate (DDB) — The Synthetic Schisandrin C Derivative as a Chinese Pharmaceutical

The most striking translational outcome of the Schisandra liver research is the development of bifendate (dimethyl-4,4'-dimethoxy-5,6,5',6'-dimethylenedioxybiphenyl-2,2'-dicarboxylate — DDB), a synthetically modified schisandrin C analog that has been a registered pharmaceutical drug in the People's Republic of China since 1982. Bifendate was developed by Chinese medicinal chemists at the Institute of Materia Medica of the Chinese Academy of Medical Sciences as a structurally simplified, more bioavailable version of the natural schisandrin C scaffold. The synthesis removes one of the methylenedioxy bridges of the natural molecule and adds two methyl ester groups that improve oral absorption.

Bifendate is licensed in China for:

• Chronic hepatitis B and C with elevated transaminases
• Drug-induced hepatitis (most commonly from antituberculosis, antiepileptic, and chemotherapeutic drugs)
• Hepatic transaminase elevation of unspecified cause

The standard dose is 7.5-15 mg orally three times daily for 4-8 weeks initially, then a maintenance phase. A 2008 review (Wang and Xu) describes bifendate as lowering alanine aminotransferase (ALT) while rarely affecting the other liver enzymes; ALT rises again when the drug is stopped, the drug has been used only as an adjuvant, and the review notes that normalizing ALT does not show a treatment benefit unless liver tissue (histology) also improves. The proposed mechanism is essentially the same as the parent schisandrin C: Nrf2 activation, glutathione upregulation, and mitochondrial stabilization, but with improved oral bioavailability and consistent pharmaceutical-grade dosing.

Bifendate is not approved by the U.S. Food and Drug Administration or the European Medicines Agency, where it has not been submitted for licensing, but it is used as an adjuvant in hepatology practice in mainland China, Hong Kong, and Taiwan, and is sometimes encountered by Western physicians treating patients of East Asian background who self-source it. The drug is widely available and reasonably priced in Chinese pharmacies and provides an interesting case study in how botanical phytochemistry can directly generate a registered pharmaceutical drug.

Back to Table of Contents

Cytochrome P450 3A4 and Drug Interactions

The clinically most important caution for Schisandra use is its effect on cytochrome P450 3A4, the single enzyme responsible for metabolizing roughly 30% of all clinically used pharmaceutical drugs. In laboratory and rodent studies, isolated Schisandra lignans induce liver drug-metabolizing enzymes: Liu and colleagues (1982) reported induction of phenobarbital-like liver monooxygenases in rats, and schisandrin B and schisantherin A are reported to activate the pregnane X receptor (PXR), a nuclear receptor that drives transcription of cytochrome P450 3A4. Those are animal and laboratory findings.

In people, the measured effect went the other way. In 12 healthy men, a Schisandra sphenanthera extract taken for 13 days raised the blood level (AUC) of the transplant drug tacrolimus by 164% on average, raised its peak level by 227%, and cut its clearance by 49% (Xin 2007). In a second study by the same group (12 healthy men, extract for 7 days), the extract raised the blood level of midazolam — the standard cytochrome P450 3A4 probe drug — by 119% and cut its clearance by 52%; the authors describe the extract as an inhibitor of CYP3A (Xin 2009). Both studies used Schisandra sphenanthera (southern schisandra, the source of the Chinese Wuzhi preparations), not Schisandra chinensis.

The clinical implication from the human studies is that Schisandra extract can raise the blood levels of co-administered cytochrome P450 3A4 substrate drugs, which for narrow-margin drugs is a toxicity risk. The two human studies measured only tacrolimus and midazolam; other drugs cleared largely by cytochrome P450 3A4 include:

• Tacrolimus and cyclosporine — transplant immunosuppressants with narrow therapeutic windows. In healthy volunteers Schisandra extract raised tacrolimus blood levels about 2.6-fold (Xin 2007); high tacrolimus levels cause kidney and nerve toxicity.
• Warfarin — cleared through CYP2C9 and CYP3A4 (the R- and S-warfarin enantiomers); its effect is tracked with the international normalized ratio (INR) blood test.
• Direct oral anticoagulants (DOACs) — apixaban and rivaroxaban are partly cytochrome P450 3A4 substrates.
• Oral contraceptives — ethinyl estradiol and many progestins are partly cleared by cytochrome P450 3A4.
• Human immunodeficiency virus (HIV) antiretrovirals — many protease inhibitors and NNRTIs are cytochrome P450 3A4 substrates with strict therapeutic-window requirements.
• Statins — simvastatin, lovastatin, and atorvastatin are cytochrome P450 3A4 substrates (pravastatin and rosuvastatin are not).
• Anticancer agents — imatinib, sunitinib, erlotinib, and other tyrosine kinase inhibitors.
• Benzodiazepines — midazolam (the standard cytochrome P450 3A4 phenotyping probe, whose blood level Schisandra extract raised about 2.2-fold in Xin 2009), triazolam, alprazolam.
• Calcium channel blockers — felodipine, amlodipine, nifedipine.

The interaction risk is highest with narrow-therapeutic-index drugs and with daily use of concentrated extract, which is what the human studies tested (7 to 13 days of capsules twice daily). Brief or occasional use of dried berries in culinary preparations was not what those studies measured.

Back to Table of Contents

Drug-Induced Liver Injury and Hepatotoxin Co-Exposure

One of the most clinically attractive applications of Schisandra is as an adjunct in drug-induced liver injury (DILI), particularly during antituberculosis therapy. Isoniazid, rifampicin, and pyrazinamide all carry meaningful hepatotoxicity risk, with clinically significant transaminase elevation in 10-20% of patients during standard 6-month combination therapy. Bifendate (the schisandrin C derivative) is routinely co-administered with antituberculosis regimens in Chinese practice and has been shown in trials to reduce transaminase elevation and reduce the need to interrupt tuberculosis (TB) therapy for hepatotoxicity. The parent extract Schisandra fruit similarly reduces transaminase elevation in patients receiving chronic chemotherapy (methotrexate, antiepileptics).

The mechanism is the same glutathione and Nrf2 upregulation discussed above — the liver tolerates the drug-induced electrophilic and oxidative stress better when its phase II conjugation capacity and antioxidant defense are augmented. The same principle has been applied to environmental hepatotoxin exposure (occupational solvents, ethanol abuse contexts), with smaller but generally favorable evidence.

One important caveat: the cytochrome P450 3A4 effect can interact unpredictably with drug-metabolism pathways. In people, Schisandra extract slowed the clearance of cytochrome P450 3A4 drugs (Xin 2007, Xin 2009), so drugs that are detoxified by this enzyme can build up to higher levels. This is a theoretical consideration in drug-DILI management.

Back to Table of Contents

Non-Alcoholic Fatty Liver Disease (NAFLD / MAFLD) Evidence

The recent (2015-2024) Schisandra literature has shifted increasingly toward non-alcoholic fatty liver disease (NAFLD), now reclassified as metabolic-dysfunction-associated fatty liver disease (MAFLD), reflecting the global epidemic of metabolic-syndrome-driven liver injury. Multiple Chinese and Korean trials have documented:

• Reduction in hepatic steatosis on ultrasound imaging
• Reduction in alanine aminotransferase and aspartate aminotransferase
• Improvement in homeostatic model assessment of insulin resistance (HOMA-IR) insulin sensitivity index
• Modest reduction in body weight and waist circumference
• Improvement in serum lipid profile (low-density lipoprotein (LDL) down, high-density lipoprotein (HDL) up modestly)

The mechanism in MAFLD likely combines the established hepatoprotective effects with secondary metabolic effects: AMP-activated protein kinase (AMPK) activation, peroxisome proliferator-activated receptor alpha (PPAR-alpha) modulation, and reduction of de novo lipogenesis. The schisandrin B effect on PPAR-alpha is particularly interesting because PPAR-alpha is the target of the fibrate class of lipid-lowering drugs.

Schisandra has been used as a MAFLD adjunct alongside the standard interventions of weight loss, exercise, and dietary modification rather than in place of them, and appears to augment their effect, similar to how Milk Thistle (silymarin) has been used as a MAFLD adjunct for several decades.

Back to Table of Contents

Practical Dosing Protocols and Standardization

Practical Schisandra dosing for liver support varies substantially depending on the preparation. A few representative regimens drawn from clinical and traditional usage:

• Dried Schisandra berry — 1.5-6 grams per day in decoction (boiled tea), the traditional Chinese preparation. The fruit is added to water and simmered 15-30 minutes; the resulting astringent reddish-brown tea is consumed throughout the day. This is the lowest-potency preparation, best used for general support and as part of a broader herbal protocol.
• Schisandra tincture (1:5 in 50% ethanol) — 2-4 mL three times daily. Tinctures extract lignans more efficiently than water decoction and provide a more concentrated dose in a more convenient format.
• Standardized lignan extract — commercially available preparations are typically standardized to either 9% schisandrins or to a specified content of schisandrin B. Typical dose is 100-500 mg of standardized extract one to three times daily, providing roughly 9-100 mg of total lignans per day.
• Bifendate (DDB) pharmaceutical — Chinese practice — 7.5-15 mg three times daily for 4-8 weeks, then maintenance dose adjusted to liver function tests.

Standardization to lignan content (preferably with schisandrin B reported separately) is the single most important quality indicator for a commercial Schisandra product. Extracts that report only "Schisandra chinensis fruit, 500 mg" without lignan content are essentially uncharacterized in pharmacological terms. A certificate of analysis, or standardized content listed on the label, is how a product shows its lignan content.

Duration of use: traditional Chinese practice uses Schisandra in 6- to 12-week courses with breaks, not continuous indefinite use. There is no formal published evidence for or against indefinite continuous use; the cytochrome P450 3A4 interaction is the main reason given for cycling rather than continuous chronic dosing.

Back to Table of Contents

Cautions and Contraindications

• Drug interactions via cytochrome P450 3A4 — as discussed in detail above, this is the dominant safety concern with Schisandra. In healthy volunteers Schisandra extract raised tacrolimus blood levels about 2.6-fold (AUC +164%) and midazolam about 2.2-fold (AUC +119%) (Xin 2007, Xin 2009). The drug classes cleared by this enzyme include immunosuppressants, some anticoagulants, oral contraceptives, antiretrovirals, several statins, anticancer agents, benzodiazepines and calcium channel blockers.
• Pregnancy and lactation — insufficient safety data in human pregnancy. Schisandra has documented uterine-stimulant effects in animal studies (it was traditionally used in late-pregnancy Chinese medicine to support labor), which is the concern raised for early and mid-pregnancy. There is no safety data for breastfeeding infants.
• Active peptic ulcer disease — Schisandra fruit is highly astringent and acidic, and case reports describe worsening of gastric ulcer pain. This concern applies to people with active peptic ulcer disease (PUD) or severe gastroesophageal reflux disease (GERD).
• Epilepsy — one of the active lignans, schisandrin A, has central nervous system-stimulant properties at high doses and has been reported to lower seizure threshold in animal models. This finding matters most for people with poorly controlled epilepsy.
• Surgical procedures — midazolam, a sedative used around surgery, reached about 2.2 times its usual blood level in healthy volunteers taking Schisandra extract (Xin 2009), which means deeper and longer sedation; fentanyl is also cleared by cytochrome P450 3A4.
• Acute hepatitis with markedly elevated transaminases (e.g., alanine aminotransferase > 10x upper limit) — Schisandra and bifendate are used as adjuncts for chronic hepatitis with moderate transaminitis, not as rescue therapy for acute hepatocellular necrosis or fulminant liver failure; jaundice, confusion and bleeding with acute hepatitis are signs of liver failure that hospitals treat as an emergency.

Back to Table of Contents

Key Research Papers

1. Liu KT, Cresteil T, Columelli S, Lesca P (1982). Pharmacological properties of dibenzo[a,c]cyclooctene derivatives isolated from Fructus Schizandrae chinensis. II. Induction of phenobarbital-like hepatic monooxygenases. Chemico-Biological Interactions 39(3):315-330. — PubMed PMID: 7074709
2. Xin HW, Wu XC, Li Q, Yu AR, Zhu M, Shen Y, Su D, Xiong L (2007). Effects of Schisandra sphenanthera extract on the pharmacokinetics of tacrolimus in healthy volunteers. British Journal of Clinical Pharmacology 64(4):469-475. — PubMed PMID: 17506780
3. Xin HW, Wu XC, Li Q, Yu AR, Xiong L (2009). Effects of Schisandra sphenanthera extract on the pharmacokinetics of midazolam in healthy volunteers. British Journal of Clinical Pharmacology 67(5):541-546. — PubMed PMID: 19552749
4. Wang C, Xu YQ (2008). Diphenyl Dimethyl Bicarboxylate in the Treatment of Viral Hepatitis, Adjuvant or Curative? Gastroenterology Research 1(1):2-7. — PubMed PMID: 27994699
5. Chiu PY, Tang MH, Mak DH, Poon MK, Ko KM (2003). Hepatoprotective mechanism of schisandrin B: role of mitochondrial glutathione antioxidant status and heat shock proteins. Free Radical Biology and Medicine 35(4):368-380. — PubMed PMID: 12899939
6. Pan SY, Dong H, Zhao XY, et al. (2008). Schisandrin B from Schisandra chinensis reduces hepatic lipid contents in hypercholesterolaemic mice. Journal of Pharmacy and Pharmacology. — PubMed PMID: 18284822
7. Panossian A, Wikman G (2008). Pharmacology of Schisandra chinensis Bail.: An overview of Russian research and uses in medicine. Journal of Ethnopharmacology 118(2):183-212. — PubMed PMID: 18515024
8. Stacchiotti A, Li Volti G, Lavazza A, Rezzani R, Rodella LF (2009). Schisandrin B stimulates a cytoprotective response in rat liver exposed to mercuric chloride. Food and Chemical Toxicology 47(11):2834-2840. — PubMed PMID: 19747521
9. Mocan A, Crisan G, Vlase L, et al. (2014). Comparative studies on polyphenolic composition, antioxidant and antimicrobial activities of Schisandra chinensis leaves and fruits. Molecules 19(9):15162-15179. — PubMed PMID: 25247685
10. Cheng N, Ren N, Gao H, Lei X, Zheng J, Cao W (2013). Antioxidant and hepatoprotective effects of Schisandra chinensis pollen extract on CCl4-induced acute liver damage in mice. Food and Chemical Toxicology. — PubMed PMID: 23201450
11. Park HJ, Lee SJ, Song Y, et al. (2014). Schisandra chinensis prevents alcohol-induced fatty liver disease in rats. Journal of Medicinal Food. — PubMed PMID: 24456360

PubMed Topic Searches

1. PubMed: Schisandra hepatoprotection
2. PubMed: Schisandrin B / glutathione / Nrf2
3. PubMed: Bifendate / DDB hepatitis trials
4. PubMed: Schisandra CYP3A4 drug interactions
5. PubMed: Schisandra NAFLD/MAFLD

Back to Table of Contents

Connections

• All Herbs
• Schisandra Overview
• Schisandra Benefits Hub
• Schisandra Adaptogenic Action
• Schisandra Cognitive Function
• Schisandra Endurance & Recovery
• Milk Thistle (Silymarin)
• Dandelion
• Glutathione
• N-Acetylcysteine
• Hepatology
• Hepatitis
• Hepatitis B
• Liver Function Tests
• Liver Cleansing
• Detoxification
• History

Back to Table of Contents

Featured Videos

×