Drugs, Chinese Herbal
Chemistry Techniques, Analytical
Cytochrome P-450 CYP1A2
Interleukin-1 stimulates Jun N-terminal/stress-activated protein kinase by an arachidonate-dependent mechanism in mesangial cells. (1/122)BACKGROUND: We have studied interleukin-1 (IL-1)-stimulated signals and gene expression in mesangial cells (MCs) to identify molecular mechanisms of MC activation, a process characteristic of glomerular inflammation. The JNK1 pathway has been implicated in cell fate decisions, and IL-1 stimulates the Jun N-terminal/stress-activated protein kinases (JNK1/SAPK). However, early postreceptor mechanisms by which IL-1 activates these enzymes remain unclear. Free arachidonic acid (AA) activates several protein kinases, and because IL-1 rapidly stimulates phospholipase A2 (PLA2) activity release AA, IL-1-induced activation of JNK1/SAPK may be mediated by AA release. METHODS: MCs were grown from collagenase-treated glomeruli, and JNK/SAPK activity in MC lysates was determined using an immunocomplex kinase assay. RESULT: Treatment of MCs with IL-1 alpha induced a time-dependent increase in JNK1/SAPK kinase activity, assessed by phosphorylation of the activating transcription factor-2 (ATF-2). Using similar incubation conditions, IL-1 also increased [3H]AA release from MCs. Pretreatment of MCs with aristolochic acid, a PLA2 inhibitor, concordantly reduced IL-1-regulated [3H]AA release and JNK1/SAPK activity, suggesting that cytosolic AA in part mediates IL-1-induced JNK1/SAPK activation. Addition of AA stimulated JNK1/SAPK activity in a time- and concentration-dependent manner. This effect was AA specific, as only AA and its precursor linoleic acid stimulated JNK1/SAPK activity. Other fatty acids failed to activate JNK1/SAPK. Pretreatment of MCs with specific inhibitors of AA oxidation by cyclooxygenase, lipoxygenase, and cytochrome P-450 epoxygenase had no effect on either IL-1- or AA-induced JNK1/SAPK activation. Furthermore, stimulation of MCs with the exogenous cyclooxygenase-, lipoxygenase-, phosphodiesterase-, and epoxygenase-derived arachidonate metabolites, in contrast to AA itself, did not activate JNK1/SAPK. CONCLUSION: We conclude that IL-1-stimulated AA release, in part, mediates stimulation of JNK1/SAPK activity and that AA activates JNK1/SAPK by a mechanism that does not require enzymatic oxygenation. JNK1 signaling pathway components may provide molecular switches that mediate structural rearrangements and biochemical processes characteristic of MC activation and could provide a novel target(s) for therapeutic intervention. (+info)
Pentoxifylline-stimulated capacitation and acrosome reaction in hamster spermatozoa: involvement of intracellular signalling molecules. (2/122)We investigated the role of cAMP/cGMP, protein kinases and intracellular calcium ( [Ca2+]i) in pentoxifylline-stimulated hamster sperm capacitation and the acrosome reaction (AR) in vitro. Treatment with pentoxifylline (0.45 mM) initially increased sperm cAMP values 2.8-fold, compared with untreated controls (396 +/- 9.2 versus 141 +/- 6.0 fmoles/10(6) spermatozoa; mean +/- SEM, n = 6) after 15 min, although by 3 h, cAMP values were similar (503-531 fmoles/10(6) spermatozoa). cGMP values ( approximately 27 fmoles/10(6) spermatozoa) were the same in treated and control spermatozoa. Both sperm capacitation and the AR, determined from the absence of an acrosomal cap, were stimulated by pentoxifylline; these were almost completely inhibited by a Cl-/ HCO3- antiporter inhibitor (4,4-diisothiocyanato-stilbene-2,2 disulphonic acid; 1 mM) defined from the degree of sperm motility and by a protein kinase A inhibitor (H89; 10 microM). A protein kinase C inhibitor (staurosporine, 1 nM) did not affect pentoxifylline-stimulated capacitation but inhibited the AR by 50%. A protein tyrosine kinase inhibitor (tyrphostin A-47, 0.1 mM) had no effect on either pentoxifylline-stimulated capacitation or AR. A phospholipase A2 inhibitor (aristolochic acid, 0.4 mM) markedly inhibited the pentoxifylline-stimulated AR but not capacitation. When intracellular sperm calcium [Ca2+/-]i was measured using fura-2-AM, there was an early rise (271 nM at 0.5 h) in pentoxifylline-treated spermatozoa; this appeared to be due to intracellular mobilization rather than to uptake. In the absence of extracellular Ca2+, sperm motility was maintained in the presence of pentoxifylline, but capacitation did not occur; spermatozoa exhibited a low level of hyperactivated motility and had a poor rate of AR (20.5 +/- 2.3%). These results suggest that: (i) the pentoxifylline-stimulated early onset of sperm capacitation may be mediated by an early rise in cAMP and [Ca2+/-]i and involves protein kinase A activity; and (ii) pentoxifylline-stimulated AR may require phospholipase A2 and protein kinase C activity. (+info)
Formation of reactive oxygen species by the contracting diaphragm is PLA(2) dependent. (3/122)Recent work indicates that respiratory muscles generate superoxide radicals during contraction (M. B. Reid, K. E. Haack, K. M. Francik, P. A. Volberg, L. Kabzik, and M. S. West. J. Appl. Physiol. 73: 1797-1804, 1992). The intracellular pathways involved in this process are, however, unknown. The purpose of the present study was to test the hypothesis that contraction-related formation of reactive oxygen species (ROS) by skeletal muscle is linked to activation of the 14-kDa isoform of phospholipase A(2) (PLA(2)). Studies were performed by using an in vitro hemidiaphragm preparation submerged in an organ bath, and formation of ROS in muscles was assessed by using a recently described fluorescent indicator technique. We examined ROS formation in resting and contracting muscle preparations and then determined whether contraction-related ROS generation could be altered by administration of various PLA(2) inhibitors: manoalide and aristolochic acid, both inhibitors of 14-kDa PLA(2); arachidonyltrifluoromethyl ketone (AACOCF(3)), an inhibitor of 85-kDa PLA(2); and haloenol lactone suicide substrate (HELSS), an inhibitor of calcium-independent PLA(2). We found 1) little ROS formation [2.0 +/- 0.8 (SE) ng/mg] in noncontracting control diaphragms, 2) a high level of ROS (20.0 +/- 2.0 ng/mg) in electrically stimulated contracting diaphragms (trains of 20-Hz stimuli for 10 min, train rate 0.25 s(-1)), 3) near-complete suppression of ROS generation in manoalide (3.0 +/- 0.5 ng/mg, P < 0. 001)- and aristolochic acid-treated contracting diaphragms (4.0 +/- 1.0 ng/mg, P < 0.001), and 4) no effect of AACOCF(3) or HELSS on ROS formation in contracting diaphragm. During in vitro studies examining fluorescent measurement of ROS formation in response to a hypoxanthine/xanthine oxidase superoxide-generating solution, manoalide, aristolochic acid, AACOCF(3), and HELSS had no effect on signal intensity. These data indicate that ROS formation by contracting diaphragm muscle can be suppressed by the administration of inhibitors of the 14-kDa isoform of PLA(2) and suggest that this enzyme plays a critical role in modulating ROS formation during muscle contraction. (+info)
W-7 induces [Ca(2+)](i) increases in Madin-Darby canine kidney (MDCK) cells. (4/122)The effect of W-7 [N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride] on Ca(2+) signaling in Madin-Darby canine kidney cells was investigated. W-7 (0.1-1 mM) induced a [Ca(2+)](i) increase, which comprised an initial increase and a plateau. Ca(2+) removal inhibited the Ca(2+) signals by 80%, suggesting that W-7 activated external Ca(2+) influx and internal Ca(2+) release. Pretreatment with the mitochondrial uncoupler carbonylcyanide m-chlorophenylhydrazone (2 microM) and the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin (1 microM) abolished the internal Ca(2+) release induced by 0.5 mM W-7; conversely, pretreatment with W-7 prevented thapsigargin and carbonylcyanide m-chlorophenylhydrazone from releasing internal Ca(2+). W-7 (0.2 mM) induced Mn(2+) quench of fura-2 fluorescence, which was inhibited by La(3+) (0.1 mM) by 80%. La(3+) (0.1 mM) partly inhibited 0.2 mM W-7-induced [Ca(2+)](i) increase. Addition of 5 mM Ca(2+) induced a significant [Ca(2+)](i) increase after pretreating with 0.2 to 1 mM W-7 in Ca(2+)-free medium for 5 min, suggesting that W-7 induced capacitative Ca(2+) entry. W-7 (0.5 mM) potentiated the capacitative Ca(2+) entry induced by 1 microM thapsigargin by 15%. Pretreatment with aristolochic acid (40 microM) to inhibit phospholipase A(2) reduced 0.5 mM W-7-induced internal Ca(2+) release and external Ca(2+) influx by 25 and 80%, respectively. Inhibition of phospholipase C with U73122 (2 microM) or inhibition of phospholipase D with propranolol (0.1 mM) had no effect on the internal Ca(2+) release induced by 0.5 mM W-7. It remains unclear whether W-7 induced [Ca(2+)](i) increases via inhibition of calmodulin. Three other calmodulin inhibitors (phenoxybenzamine, trifluoperazine, and fluphenazine-N-chloroethane) did not alter resting [Ca(2+)](i). (+info)
Using polymerase arrest to detect DNA binding specificity of aristolochic acid in the mouse H-ras gene. (5/122)The distribution of DNA adducts formed by the two main components, aristolochic acid I (AAI) and aristolochic acid II (AAII), of the carcinogenic plant extract aristolochic acid (AA) was examined in a plasmid containing exon 2 of the mouse c-H-ras gene by a polymerase arrest assay. AAI and AAII were reacted with plasmid DNA by reductive activation and the resulting DNA adducts were identified as the previously characterized adenine adducts (dA-AAI and dA-AAII) and guanine adducts (dG-AAI and dG-AAII) by the (32)P-post-labeling method. In addition, a structurally unknown adduct was detected in AAII-modified DNA and shown to be derived from reaction with cytosine (dC-AAII). Sites at which DNA polymerase progress along the template was blocked were assumed to be at the nucleotide 3' to the adduct. Polymerase arrest spectra showed a preference for reaction with purine bases in the mouse H-ras gene for both activated compounds, consistent with previous results that purine adducts are the principal reaction products of AAI and AAII with DNA. Despite the structural similarities among AAI-DNA and AAII-DNA adducts, however, the polymerase arrest spectra produced by the AAs were different. According to the (32)P-post-labeling analyses reductively activated AAI showed a strong preference for reacting with guanine residues in plasmid DNA, however, the polymerase arrest assay revealed arrest sites preferentially at adenine residues. In contrast, activated AAII reacted preferentially with adenine rather than guanine residues and to a lesser extent with cytosine but DNA polymerase was arrested at guanine as well as adenine and cytosine residues with nearly the same average relative intensity. Thus, the polymerase arrest spectra obtained with the AA-adducted ras sequence do not reflect the DNA adduct distribution in plasmid DNA as determined by (32)P-post-labeling. Arrest sites of DNA polymerase associated with cytosine residues confirmed the presence of a cytosine adduct in DNA modified by AAII. For both compounds adduct distribution was not random; instead, regions with adduct hot spots and cold spots were observed. Results from nearest neighbor binding analysis indicated that flanking pyrimidines displayed the greatest effect on polymerase arrest and therefore on DNA binding by AA. (+info)
Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2. (6/122)Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists. (+info)
Effects of inhibitors of arachidonic acid turnover on the production of prostaglandins by the guinea-pig uterus. (7/122)The supply of free arachidonic acid from phospholipids is generally regarded as the rate-limiting step for prostaglandin (PG) synthesis by tissues. Two enzymes involved in arachidonic acid uptake into, and release from, phospholipids are acyl-CoA:lysophospholipid acyltransferase (ACLAT) and phospholipase A2 (PLA2), respectively. PGF2 alpha produced by the endometrium induces luteolysis in several species including guinea-pigs. Thimerosal, an inhibitor of ACLAT, and aristolochic acid, an inhibitor of PLA2, both reduced, in a concentration-dependent manner, the output of PGF2 alpha from guinea-pig endometrium cultured for 24 h on days 7 and 15 of the oestrous cycle. This study showed that the continual production of PGF 2 alpha by guinea-pig endometrium is not only dependent upon the activity of PLA2 for releasing free arachidonic acid for PGF2 alpha synthesis, but also on the incorporation of arachidonic acid into the phospholipid pool by the activity of ACLAT. The inhibitory effects of thimerosal and aristolochic acid on the outputs of PGE2 and 6-keto-PGF1 alpha were less marked, particularly on day 7 when the low output of PGE2 was unaffected and the output of 6-keto-PGF1 alpha was increased at the lower concentrations of thimerosal. This finding indicates that there are different pools of arachidonic acid bound as phospholipid for the syntheses of PGF2 alpha and 6-keto-PGF1 alpha by guinea-pig endometrium. (+info)
Urothelial carcinoma associated with the use of a Chinese herb (Aristolochia fangchi) (8/122)BACKGROUND: Chinese-herb nephropathy is a progressive form of renal fibrosis that develops in some patients who take weight-reducing pills containing Chinese herbs. Because of a manufacturing error, one of the herbs in these pills (Stephania tetrandra) was inadvertently replaced by Aristolochia fangchi, which is nephrotoxic and carcinogenic. METHODS: The diagnosis of a neoplastic lesion in the native urinary tract of a renal-transplant recipient who had Chinese-herb nephropathy prompted us to propose regular cystoscopic examinations and the prophylactic removal of the native kidneys and ureters in all our patients with end-stage Chinese-herb nephropathy who were being treated with either transplantation or dialysis. Surgical specimens were examined histologically and analyzed for the presence of DNA adducts formed by aristolochic acid. All prescriptions written for Chinese-herb weight-reducing compounds during the period of exposure (1990 to 1992) in these patients were obtained, and the cumulative doses were calculated. RESULTS: Among 39 patients who agreed to undergo prophylactic surgery, there were 18 cases of urothelial carcinoma (prevalence, 46 percent; 95 percent confidence interval, 29 to 62 percent): 17 cases of carcinoma of the ureter, renal pelvis, or both and 1 papillary bladder tumor. Nineteen of the remaining patients had mild-to-moderate urothelial dysplasia, and two had normal urothelium. All tissue samples analyzed contained aristolochic acid-related DNA adducts. The cumulative dose of aristolochia was a significant risk factor for urothelial carcinoma, with total doses of more than 200 g associated with a higher risk of urothelial carcinoma. CONCLUSIONS: The prevalence of urothelial carcinoma among patients with end-stage Chinese-herb nephropathy (caused by aristolochia species) is a high. (+info)
The exact cause of Balkan nephropathy is not known, but it is believed to be linked to a combination of genetic and environmental factors, including poor nutrition, alcohol consumption, and exposure to certain toxins. The disease is more common in males than females and typically affects people in their 20s to 40s.
Symptoms of Balkan nephropathy can include proteinuria (excess protein in the urine), hematuria (blood in the urine), and kidney failure. Treatment options are limited and may include medications to control hypertension and proteinuria, as well as dialysis or kidney transplantation in advanced cases.
Balkan nephropathy is an important health problem in the regions where it is prevalent, and further research is needed to understand its causes and develop effective prevention and treatment strategies.
Some common types of urologic neoplasms include:
1. Renal cell carcinoma (RCC): a type of kidney cancer that originates in the cells of the kidney's tubules.
2. Bladder cancer: a type of cancer that affects the cells lining the bladder, and can be classified as superficial or invasive.
3. Ureteral cancer: a rare type of cancer that develops in the muscular tissue of the ureters.
4. Prostate cancer: a common type of cancer in men that affects the prostate gland.
5. Penile cancer: a rare type of cancer that develops on the penis, usually in the skin or mucous membranes.
6. Testicular cancer: a rare type of cancer that develops in the testicles, and is most common in young men between the ages of 15 and 35.
The symptoms of urologic neoplasms can vary depending on their location and size, but may include blood in the urine, painful urination, frequent urination, or abdominal pain. Diagnosis is typically made through a combination of imaging studies (such as CT scans or ultrasound) and tissue biopsy.
Treatment options for urologic neoplasms vary depending on the type, size, location, and stage of the tumor, but may include surgery, chemotherapy, radiation therapy, or a combination of these. In some cases, watchful waiting or active surveillance may be recommended for small, slow-growing tumors that are not causing symptoms or threatening the patient's life.
The prognosis for urologic neoplasms varies depending on the type and stage of the cancer at the time of diagnosis. In general, early detection and treatment improve the chances of a successful outcome. However, some types of urologic neoplasms are more aggressive and difficult to treat than others.
Prevention is often challenging for urologic neoplasms, as many risk factors (such as family history or genetic predisposition) cannot be controlled. However, some measures may help reduce the risk of developing certain types of urologic neoplasms, such as:
* Maintaining a healthy diet and lifestyle
* Avoiding smoking and excessive alcohol consumption
* Protecting the skin from sun exposure to reduce the risk of skin cancer
* Avoiding exposure to certain chemicals or toxins that may increase the risk of certain types of cancer
* Practicing safe sex to reduce the risk of HPV-related cancers.
There are several types of urethral neoplasms, including:
1. Urethral papillomas: These are small, non-cancerous growths that resemble a wart and typically occur in the distal (outer) part of the urethra.
2. Urethral polyps: These are soft, growths that can occur in any part of the urethra and are usually benign.
3. Urethral carcinomas: These are malignant tumors that arise from the epithelial lining of the urethra. They can be superficial (confined to the surface) or invasive (penetrate deeper into the tissue).
4. Urethral melanoma: This is a rare type of malignant tumor that arises from the pigment-producing cells of the urethra. It is more common in men than women and typically affects the distal part of the urethra.
The symptoms of urethral neoplasms can vary depending on the size and location of the growth, but may include:
* Blood in the urine
* Painful urination
* Frequent urination
* Difficulty starting or stopping the flow of urine
* Pain in the pelvic area
Diagnosis of urethral neoplasms typically involves a combination of physical examination, urine cytology (examination of cells in the urine), and imaging studies such as ultrasound or MRI. A biopsy may also be performed to confirm the diagnosis.
Treatment options for urethral neoplasms depend on the type and location of the growth, but may include:
* Surgery to remove the tumor
* Cryotherapy (freezing of the tumor)
* Laser therapy
* Chemotherapy or radiation therapy for more advanced cases
Early detection and treatment of urethral neoplasms are important to improve outcomes and minimize complications. Regular screening and follow-up with a healthcare provider can help identify any abnormalities in the urinary tract and allow for prompt treatment if needed.
Types of Kidney Diseases:
1. Acute Kidney Injury (AKI): A sudden and reversible loss of kidney function that can be caused by a variety of factors, such as injury, infection, or medication.
2. Chronic Kidney Disease (CKD): A gradual and irreversible loss of kidney function that can lead to end-stage renal disease (ESRD).
3. End-Stage Renal Disease (ESRD): A severe and irreversible form of CKD that requires dialysis or a kidney transplant.
4. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste products.
5. Interstitial Nephritis: An inflammation of the tissue between the tubules and blood vessels in the kidneys.
6. Kidney Stone Disease: A condition where small, hard mineral deposits form in the kidneys and can cause pain, bleeding, and other complications.
7. Pyelonephritis: An infection of the kidneys that can cause inflammation, damage to the tissues, and scarring.
8. Renal Cell Carcinoma: A type of cancer that originates in the cells of the kidney.
9. Hemolytic Uremic Syndrome (HUS): A condition where the immune system attacks the platelets and red blood cells, leading to anemia, low platelet count, and damage to the kidneys.
Symptoms of Kidney Diseases:
1. Blood in urine or hematuria
2. Proteinuria (excess protein in urine)
3. Reduced kidney function or renal insufficiency
4. Swelling in the legs, ankles, and feet (edema)
5. Fatigue and weakness
6. Nausea and vomiting
7. Abdominal pain
8. Frequent urination or polyuria
9. Increased thirst and drinking (polydipsia)
10. Weight loss
Diagnosis of Kidney Diseases:
1. Physical examination
2. Medical history
3. Urinalysis (test of urine)
4. Blood tests (e.g., creatinine, urea, electrolytes)
5. Imaging studies (e.g., X-rays, CT scans, ultrasound)
6. Kidney biopsy
7. Other specialized tests (e.g., 24-hour urinary protein collection, kidney function tests)
Treatment of Kidney Diseases:
1. Medications (e.g., diuretics, blood pressure medication, antibiotics)
2. Diet and lifestyle changes (e.g., low salt intake, increased water intake, physical activity)
3. Dialysis (filtering waste products from the blood when the kidneys are not functioning properly)
4. Kidney transplantation ( replacing a diseased kidney with a healthy one)
5. Other specialized treatments (e.g., plasmapheresis, hemodialysis)
Prevention of Kidney Diseases:
1. Maintaining a healthy diet and lifestyle
2. Monitoring blood pressure and blood sugar levels
3. Avoiding harmful substances (e.g., tobacco, excessive alcohol consumption)
4. Managing underlying medical conditions (e.g., diabetes, high blood pressure)
5. Getting regular check-ups and screenings
Early detection and treatment of kidney diseases can help prevent or slow the progression of the disease, reducing the risk of complications and improving quality of life. It is important to be aware of the signs and symptoms of kidney diseases and seek medical attention if they are present.
Standard for the Uniform Scheduling of Medicines and Poisons
List of traditional Chinese medicines
Balkan endemic nephropathy
Battus philenor hirsuta
Queen Alexandra's birdwing
List of herbs with known adverse effects
IARC group 1
Aristolochic acid-associated urothelial cancer in Taiwan - PubMed
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MECHANISMS UNDERLYING ACTIVATION AND DETOXIFICATION OF ARISTOLOCHIC ACIDS IN HUMAN HEPATIC AND RENAL CELLS
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- Aristolochic acid, a potent human carcinogen produced by Aristolochia plants, is associated with urothelial carcinoma of the upper urinary tract (UUC). (nih.gov)
- Aristolochic acids (AA), principal components of Aristolochia plants used worldwide for medicinal purposes, are potent carcinogens and nephrotoxins. (nih.gov)
- Abstract Aristolochic acids (AAs) are the active components of herbal drugs derived from Aristolochia species that have been used for medicinal purposes since antiquity. (ljmu.ac.uk)
- Aristolochic acid (AA) is an abundant chemical substance commonly present in the genus, Aristolochia . (hh-publisher.com)
- A review of the degradation work carried out on aristolochic acids is given followed by an account of the pharmacological activity of extracts and compounds isolated from Aristolochia species. (gla.ac.uk)
- Research published last week in the medical journal Science Translational Medicine has identified several traditional medications that included Aristolochia and related plants that contain nephrotoxins and mutagens in the form of aristolich acids (AA) and other similar compounds, which may be linked to kidney problems. (aboutlawsuits.com)
- Forms of aristolich acids are found in aristolochia and as arum plants that are used in a wide variety of every-day use medications across Asia for slimming and weight loss. (aboutlawsuits.com)
- and aristolochic acid, which comes from the herb Aristolochia clematitis . (nih.gov)
- Aristolochic acid found its way into the food supply through bread contaminated with Aristolochia clematitis , a weed accidentally harvested along with wheat grown in the area. (nih.gov)
- Following metabolic activation, aristolochic acid reacts with DNA to form aristolactam (AL)-DNA adducts. (nih.gov)
- 11. Analyses of DNA adducts formed by ochratoxin A and aristolochic acid in patients with Chinese herbs nephropathy. (nih.gov)
- 13. Exceptionally long-term persistence of DNA adducts formed by carcinogenic aristolochic acid I in renal tissue from patients with aristolochic acid nephropathy. (nih.gov)
- Turesky was able to identify the aristolochic acid-DNA adducts using mass spectrometry techniques that proved these adducts were responsible for the mutational pattern. (nih.gov)
- 1 Voting member of the riddelliine panel but a non- member, technical expert for the aristolochic-related exposure panel. (nih.gov)
- The unusual high dialysis prevalence and upper urinary tract urothelial carcinoma (UTUC) incidence in Taiwan may attribute to aristolochic acid (AA), which is nephrotoxic and carcinogenic, exposure. (figshare.com)
- Background: Both aristolochic acid (AA) exposure and diabetic can increase risk of certain cancers,whetherAAexposureincreases cancer risk in diabetic patientsisunknown. (tmu.edu.tw)
- 20. Aristolochic acid (AA)-DNA adduct as marker of AA exposure and risk factor for AA nephropathy-associated cancer. (nih.gov)
- Researchers led by Steven Rozen, professor of Duke-NUS Medical School in Singapore, began to examine patients at a Taiwan hospital and found that of the 98 patients with liver tumors, 78 percent showed signs indicating exposure to aristolich acid compounds. (aboutlawsuits.com)
- Scientists pulled global data to examine 1,400 liver cancer mutations and found that 47 percent of case found in China and 29 percent recorded in Southeast Asia showed evidence of exposure to aristolich acid compounds. (aboutlawsuits.com)
- Other countries showed evidence of exposure among their rates of liver cancer as well, with aristolich acid suspected of being a contributing factor of 13 percent of liver cancer cases in Korea, 2.7 percent in Japan, 4.8 percent in North America, and 1.7 Europe. (aboutlawsuits.com)
- The findings here indicate that exposure to aristolochic acids and their derivatives is geographically widespread, implying substantial opportunities for primary and secondary prevention," the researchers determined. (aboutlawsuits.com)
- The cause of a kidney disease particular to the Balkans was a mystery until a group of researchers, including Turesky, showed that exposure to aristolochic acid was the culprit. (nih.gov)
- As the carcinogenic risk of herbs containing aristolochic acids (AAs) is a global health issue, quantitative evaluation of toxicity is needed for the regulatory decision -making and risk assessment of AAs. (bvsalud.org)
- Balkan endemic nephropathy (BEN), an environmental form of aristolochic acid nephropathy is characterized with later onset and milder forms of hypertension (HT). (mef.hr)
- 2. Aristolochic acid and 'Chinese herbs nephropathy': a review of the evidence to date. (nih.gov)
- 3. Aristolochic acid nephropathy: a worldwide problem. (nih.gov)
- 5. [Aristolochic acid nephropathy]. (nih.gov)
- 7. An Integrated View of Aristolochic Acid Nephropathy: Update of the Literature. (nih.gov)
- 8. [Nephropathy caused by Chinese plants and aristolochic acids: from clinical observation to experimental model]. (nih.gov)
- 10. Effects of dexfenfluramine on aristolochic acid nephrotoxicity in a rat model for Chinese-herb nephropathy. (nih.gov)
- 14. Chronic aristolochic acid toxicity in rabbits: a model of Chinese herbs nephropathy? (nih.gov)
- 17. De novo urothelial carcinoma in kidney transplant patients with end-stage aristolochic acid nephropathy in China. (nih.gov)
- 19. [Case of traditional herbal medicine-induced aristolochic acid nephropathy developing to end-stage renal failure]. (nih.gov)
- Endemic (Balkan) nephropathy (EN) involves chronic kidney failure and is strongly associated with cancer of the upper urinary tract. (nih.gov)
- 18. Aristolochic acid-induced upper tract urothelial carcinoma in Taiwan: clinical characteristics and outcomes. (nih.gov)
- After a report on the synthesis of derivatives of aristolochic acid, in which the benzoate of 8-methoxy-3,4-methylendioxy-10-nitro-l-phenanthroic lactam was obtained as the only new product, a route to aristolochic acid is proposed. (gla.ac.uk)
- One particularly troublesome ingredient, aristolochic acid, is commonly used in traditional remedies and has been linked to fatal kidney damage and cancers of the urinary tract. (scientificamerican.com)
- A popular plant originating from the southeastern European region known as the Balkans is found to possess toxic attributes in the form of compounds known as artistolochic acids. (healthykidneyinc.com)
- 12. Fanconi's syndrome, interstitial fibrosis and renal failure by aristolochic acid in Chinese herbs. (nih.gov)
- Aristolochic acid (AA), a mixture of aristolochic acid I (AAI) and aristolochic acid II (AAII), is present in Aristolochiaceae plants, many of which are used as herbal folk remedies. (jfda-online.com)
- New findings about an herbal component called aristolochic acid, which is found in a plant used in herbal remedies for thousands of years, is proof that just because something has been used for millennia or is natural doesn't mean that it's safe. (prostate.net)
- 9. Aristolochic acid as a probable human cancer hazard in herbal remedies: a review. (nih.gov)
- RÉSUMÉ Afin d'atteindre les objectifs de santé fixés par le pays pour 2011-2016, une analyse qualitative de l'exposition aux facteurs de risque de cancer au Qatar a été conduite en 2013. (who.int)
- Les risques de cancer les plus élevés pour les Qatariens proviendraient de facteurs associés aux modes de vie, en particulier l'obésité, la sédentarité et le tabagisme. (who.int)
- Hepatic cytochrome P450s (CYPs) play an important role in the metabolism of plant carcinogen, aristolochic acid I (AAI). (biomedcentral.com)
- Chemical examination of aqueous extracts of the starch showed the presence of choline, glucose, maltose, azelaic acid and aminoacids. (gla.ac.uk)
- 3. Aristolochic acid mutational signature defines the low-risk subtype in upper tract urothelial carcinoma. (nih.gov)
- 8. Aristolochic acid-induced upper tract urothelial carcinoma in Taiwan: clinical characteristics and outcomes. (nih.gov)
- 13. Toward clinical understanding of aristolochic acid upper-tract urothelial carcinoma. (nih.gov)
- 15. Aristolochic Acid Affects Upper Tract Urothelial Cancer Behavior through the MAPK Pathway. (nih.gov)
- 16. Aristolochic Acid and Immunotherapy for Urothelial Carcinoma: Directions for unmet Needs. (nih.gov)
- aristolochic acid personal communication, August 2017). (who.int)
- This comprehensive study aims to strengthen the case for the implementation of prevention measures against the multifaceted, detrimental, and potentially fully preventable effects of aristolochic acids on the development of cancer in humans. (who.int)
- 14. Additive Effects of Arsenic and Aristolochic Acid in Chemical Carcinogenesis of Upper Urinary Tract Urothelium. (nih.gov)
- To identify enzymes involved in the metabolism of aristolochic acid I (AAI), the major toxic component of AA we used HRN (hepatic cytochrome P450 [Cyp] reductase null) mice, in which NADPH:Cyp oxidoreductase (Por) is deleted in hepatocytes. (icr.ac.uk)
- Aristolochic acids are a group of naturally occurring compounds that are present in many plant species of the family Aristolochiaceae. (who.int)
- In a new article published in the journal Nature Reviews Cancer , scientists from the International Agency for Research on Cancer (IARC) and partner institutions review the latest evidence for the mutagenicity and carcinogenicity of aristolochic acids. (who.int)