| Erysimum crepidifolium | |
|---|---|
 | |
Scientific classification  | |
| Kingdom: | Plantae |
| Clade: | Tracheophytes |
| Clade: | Angiosperms |
| Clade: | Eudicots |
| Clade: | Rosids |
| Order: | Brassicales |
| Family: | Brassicaceae |
| Genus: | Erysimum |
| Species: | E. crepidifolium |
| Binomial name | |
| Erysimum crepidifolium | |
Erysimum crepidifolium, the pale wallflower, is a plant species in the crucifer family, Brassicaceae. It is a member of the genus Erysimum , which includes between 150 and 350 species in the Northern Hemisphere. [1]
Erysimum crepidifolium is an annual to short-lived perennial herbaceous plant that has upright stems, reaching a height of up to 60 cm. The leaves are hirsute, with margins ranging from dentate to entire.
Flowering occurs primarily from April until July. More rarely, E. crepidifolium plants also produce flowers in the fall.The odorless flowers are relatively large, reaching lengths of 9 to 15 mm. The four petals have a pale yellow color. There are six anthers. The 20 to 70 mm seed pods are gray-green, four-sided with rounded corners, and have 3 to 5 mm stems.
The species has a 2n = 14 chromosome number. [2]
E. crepidifolium is most easily confused with Erysimum odoratum Ehrh. (syn. Erysimum hieraciifolium L.), [3] [4] and with Erysimum marschallianum Andrz. ex DC. (E. marschallianum, itself, is cited by Malyschev and Peschkova as E. hieraciifolium) [lower-alpha 1] The latter, E. marschallianum, is differentiated primarily by the shape of the trichomes.
Erysimum crepidifolium grows in dry meadows, preferring warm, rocky soils. [2] The species occurs naturally from the Balkans and Italy [6] to southern and central Germany. However, it is uncommon in Germany, where it is found most frequently in the middle Saale and Nahe river valleys. [7] [8] Other reported sites are in northern Bavaria and southwestern Germany. It is not native in Switzerland [9] or Austria. [10]
Like most members of the genus Erysimum , E. crepidifolium contains both cardiac glycosides (cardenolides), [11] [12] [13] and glucosinolates. [14]
All parts of E. crepidifolium are toxic due to their cardenolide content. There are at least 20 different cardenolides in the seeds, making up ~3.5% of the total mass. Among these, the most common are erysimoside (~2.3%) and its deglycosylated form helveticoside (0.5–1.2%). [11] [12] The highest concentrations of erysimoside and helveticoside are found during ripening and in drying seeds. [15] Among 48 tested Erysimum species,E. crepidifolium had the highest cardenolide content in the leaves, at least three-fold higher than any of the other species. [16]
Toxicity in humans has not been reported, though mass die-offs of geese are known. Consumption of E. crepidifolium by geese leads to muscle paralysis from which the animals eventually die (hence the German common name "Gänsesterbe“, or geese death, for this species). Rabbits are also considered susceptible, but chickens are reportedly resistant to E. crepidifolium toxicity. [15] [17]
Due to its close phylogenetic relationship with the well-studied model plant species Arabidopsis thaliana, E. crepidifolium has been proposed as a suitable system for investigating the cardenolide biosynthetic pathway. [18] Progesterone 5β-reductase, which was initially proposed as an enzyme of cardenolide biosynthesis in Digitalis, also has been cloned from E. crepidifolium. [18] However, the natural substrate of this E. crepidifolium enzyme has not yet been identified. 3β-Hydroxysteroid dehydrogenases represent another enzyme class that is predicted to be involved in cardenolide biosynthesis. Comparison to A. thaliana genes identified three predicted 3β-hydroxysteroid dehydrogenases in E. crepidifolium (EcHSD1,EcHSD2, and EcHSD3). [19] In vitro assays showed that all three enzymes catalyze the dehydrogenation of pregnenolone and the 3-reduction of 5-α/β-pregnane-3,20-dione. Whereas EcHSD1 expression was not induced by tested stress conditions, EcHSD2 expression was upregulated by osmotic stress, and EcHSD3 expression was upregulated by both osmotic stress and treatment with methyl jasmonate, an endogenous elicitor of chemical defenses in many plant species. [20] Successful propagation of E. crepidifolium as shoot cultures allows the production of uniform plant material for in vitro assays. [21] Expression of two progesterone 5β-reductase and three 3β-hydroxysteroid dehydrogenase genes was detected in shoot cultures. [21]
Erysimum, or wallflower, is a genus of flowering plants in the cabbage family, Brassicaceae. It includes more than 150 species, both popular garden plants and many wild forms. The genus Cheiranthus is sometimes included here in whole or in part. Erysimum has since the early 21st century been ascribed to a monogeneric cruciferous tribe, Erysimeae, characterised by sessile, stellate (star-shaped) and/or malpighiaceous (two-sided) trichomes, yellow to orange flowers and multiseeded siliques.
11β-Hydroxysteroid dehydrogenase enzymes catalyze the conversion of inert 11 keto-products (cortisone) to active cortisol, or vice versa, thus regulating the access of glucocorticoids to the steroid receptors.
11β-Hydroxysteroid dehydrogenase type 1, also known as cortisone reductase, is an NADPH-dependent enzyme highly expressed in key metabolic tissues including liver, adipose tissue, and the central nervous system. In these tissues, HSD11B1 reduces cortisone to the active hormone cortisol that activates glucocorticoid receptors. It belongs to the family of short-chain dehydrogenases.
3β-Hydroxysteroid dehydrogenase/Δ5-4 isomerase (3β-HSD) is an enzyme that catalyzes the biosynthesis of the steroid progesterone from pregnenolone, 17α-hydroxyprogesterone from 17α-hydroxypregnenolone, and androstenedione from dehydroepiandrosterone (DHEA) in the adrenal gland. It is the only enzyme in the adrenal pathway of corticosteroid synthesis that is not a member of the cytochrome P450 family. It is also present in other steroid-producing tissues, including the ovary, testis and placenta. In humans, there are two 3β-HSD isozymes encoded by the HSD3B1 and HSD3B2 genes.
17β-Hydroxysteroid dehydrogenase III deficiency is a rare autosomal recessive disorder of sexual development condition that is a cause of 46,XY disorder of sex development. The impaired testosterone biosynthesis by 17β-hydroxysteroid dehydrogenase III, presents as atypical genitalia in affected males.
17β-Hydroxysteroid dehydrogenases, also 17-ketosteroid reductases (17-KSR), are a group of alcohol oxidoreductases which catalyze the reduction of 17-ketosteroids and the dehydrogenation of 17β-hydroxysteroids in steroidogenesis and steroid metabolism. This includes interconversion of DHEA and androstenediol, androstenedione and testosterone, and estrone and estradiol.
In enzymology, a 20-α-hydroxysteroid dehydrogenase (EC 1.1.1.149) is an enzyme that catalyzes the chemical reaction
In enzymology, a 3alpha(or 20beta)-hydroxysteroid dehydrogenase (EC 1.1.1.53) is an enzyme that catalyzes the chemical reaction
Erysimum cheiranthoides, the treacle-mustard,wormseed wallflower, or wormseed mustard is a species of Erysimum native to most of central and northern Europe and northern and central Asia. Like other Erysimum species, E. cheiranthoides accumulates two major classes of defensive chemicals, glucosinolates and cardiac glycosides.
17β-Hydroxysteroid dehydrogenase 1 (17β-HSD1) is an enzyme that in humans is encoded by the HSD17B1 gene. This enzyme oxidizes or reduces the C17 hydroxy/keto group of androgens and estrogens and hence is able to regulate the potency of these sex steroids
Aldo-keto reductase family 1 member C3 (AKR1C3), also known as 17β-hydroxysteroid dehydrogenase type 5 is a key steroidogenic enzyme that in humans is encoded by the AKR1C3 gene.
17-β-Hydroxysteroid dehydrogenase X (HSD10) also known as 3-hydroxyacyl-CoA dehydrogenase type-2 is a mitochondrial enzyme that in humans is encoded by the HSD17B10 gene. Several alternatively spliced transcript variants have been identified, but the full-length nature of only two transcript variants has been determined. Human HSD10 cDNA was cloned from brain (NM_004493), and the resulting protein, a homotetramer, was first characterized as a short chain 3-hydroxyacyl-CoA dehydrogenase (SCHAD). Active sites of this enzyme can accommodate different substrates; 17β-HSD10 is involved in the oxidation of isoleucine, branched-chain fatty acids, and xenobiotics as well as the metabolism of sex hormones and neuroactive steroids.
17β-Hydroxysteroid dehydrogenase 2 (17β-HSD2) is an enzyme of the 17β-hydroxysteroid dehydrogenase (17β-HSD) family that in humans is encoded by the HSD17B2 gene.
3α-Hydroxysteroid dehydrogenase is an enzyme that in humans is encoded by the AKR1C4 gene. It is known to be necessary for the synthesis of the endogenous neurosteroids allopregnanolone, THDOC, and 3α-androstanediol. It is also known to catalyze the reversible conversion of 3α-androstanediol (5α-androstane-3α,17β-diol) to dihydrotestosterone and vice versa.
3-keto-steroid reductase is an enzyme that in humans is encoded by the HSD17B7 gene.
17β-Hydroxysteroid dehydrogenase 3 (17β-HSD3) is an enzyme that in humans is encoded by the HSD17B3 gene and is involved in androgen steroidogenesis.
Cortisone reductase deficiency is caused by dysregulation of the 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1), otherwise known as cortisone reductase, a bi-directional enzyme, which catalyzes the interconversion of cortisone to cortisol in the presence of NADH as a co-factor. If levels of NADH are low, the enzyme catalyses the reverse reaction, from cortisol to cortisone, using NAD+ as a co-factor.
Cortisol is a glucocorticoid that plays a variety of roles in many different biochemical pathways, including, but not limited to: gluconeogenesis, suppressing immune system responses and carbohydrate metabolism.
One of the symptoms of cortisone reductase deficiency is hyperandrogenism, resulting from activation of the Hypothalamic–pituitary–adrenal axis. The deficiency has been known to exhibit symptoms of other disorders such as Polycystic Ovary Syndrome in women. Cortisone Reductase Deficiency alone has been reported in fewer than ten cases in total, all but one case were women. Elevated activity of 11β-HSD1 can lead to obesity or Type II Diabetes, because of the role of cortisol in carbohydrate metabolism and gluconeogenesis.
20α-Dihydroprogesterone (20α-DHP), also known as 20α-hydroxyprogesterone (20α-OHP), is a naturally occurring, endogenous progestogen. It is a metabolite of progesterone, formed by the 20α-hydroxysteroid dehydrogenases (20α-HSDs) AKR1C1, AKR1C2, and AKR1C3 and the 17β-hydroxysteroid dehydrogenase (17β-HSD) HSD17B1. 20α-DHP can be transformed back into progesterone by 20α-HSDs and by the 17β-HSD HSD17B2. HSD17B2 is expressed in the human endometrium and cervix among other tissues. In animal studies, 20α-DHP has been found to be selectively taken up into and retained in target tissues such as the uterus, brain, and skeletal muscle.
11α-Hydroxyprogesterone (11α-OHP), or 11α-hydroxypregn-4-ene-3,20-dione is an endogenous steroid and metabolite of progesterone. It is a weak antiandrogen, and is devoid of androgenic, estrogenic, and progestogenic activity. It was investigated as a topical antiandrogen for the treatment of androgen-dependent skin conditions in the early 1950s, and was found to produce some benefit. In 1995, 11α-OHP, along with its epimer 11β-hydroxyprogesterone, was identified as a very potent competitive inhibitor of both isoforms (1 and 2) of 11β-hydroxysteroid dehydrogenase (11β-HSD). It is notably not metabolized by 11β-HSD2. 11α-OHP is a more potent inhibitor of 11β-HSD than enoxolone (glycyrrhetinic acid) or carbenoxolone in vitro (IC50 = 0.9 nM; IC50 = 5 nM in transfected cells). The compound has been found to be highly active in conferring mineralocorticoid sodium-retaining activity of corticosterone in vivo in rat bioassays and in increasing blood pressure, effects that it mediates by preventing the 11β-HSD-mediated inactivation of endogenous corticosteroids. Because of its inhibition of 11β-HSD and consequent potentiation of corticosteroids, 11α-OHP has recently been patented for the treatment of skin diseases, particularly psoriasis in combination with clobetasol propionate and minoxidil.
Erysimum collinum is a plant species in the family Brassicaceae. It is a member of the genus Erysimum, which includes between 150 and 350 species in the Northern Hemisphere.