Steroid biotransformation ppt

Transdermal patches (adhesive patches placed on the skin) may also be used to deliver a steady dose through the skin and into the bloodstream. Testosterone-containing creams and gels that are applied daily to the skin are also available, but absorption is inefficient (roughly 10%, varying between individuals) and these treatments tend to be more expensive. Individuals who are especially physically active and/or bathe often may not be good candidates, since the medication can be washed off and may take up to six hours to be fully absorbed. There is also the risk that an intimate partner or child may come in contact with the application site and inadvertently dose himself or herself; children and women are highly sensitive to testosterone and can suffer unintended masculinization and health effects, even from small doses. Injection is the most common method used by individuals administering AAS for non-medical purposes. [45]

Elimination ENG is eliminated with a mean half-life of approximately 30 hours, with no difference between single and multiple dosing. Steady-state levels in plasma are reached after 4-5 days. The serum clearance after . administration of ENG is approximately 10 l per hour. Excretion of ENG and its metabolites either as free steroid or as conjugates, is with urine and faeces (ratio :1). In lactating women, ENG is excreted in breast milk with a milk/serum ratio of -. Based on these data and an estimated milk intake of 150 ml/kg/day, - microgram etonogestrel maybe ingested by the infant.




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Protection against one particular research toxin (7,12-DMBA) has been noted with acute usage of 9mmol/kg calcium-D-glucarate ( 3 hours prior to and another dose 30 minutes prior to DMBA injections) which reduced tumor occurrence from 100% to 30% [7] and studies with more chronic loading have noted benefit with dietary supplementation of 75mmol/kg (of the diet, /kg bodyweight and 213mg/kg human equivalent). [1] [7] This protective effect extends beyond breast cancer and is able to attenuate skin cancer with either calcium-D-glucarate itself [22] or the main bioactive metabolite [23] (skin cancer is known to be able to be induced by DMBA [24] ) and may also extend to DMBA induced oral cancers. [25]

As indicated in the Figure above showing the pathway of cholesterol biosynthesis a molecule of geranylpyrophosphate (GPP) and a molecule of isopentenylpyrophosphate (IPP) are condensed into farnesylpyrophosphate (FPP) through the action of the farnesyl diphosphate synthase enzyme which is encoded by the FDPS gene. Through the action of the ER-localized enzyme, dehydrodolichyl diphosphate synthase (encoded by the DHDDS gene), farnesylpyrophosphate is elongated via the sequential head-to-tail addition of multiple isopentenylpyrophosphate groups in a reaction referred to as cis -prenylation. The number of IPP substrates added ultimately determines the overall number of isoprene units in dolichol which in humans ranges from 17 to 21. The DHDDS gene is located on chromosome and is composed of 10 exons that generate five alternatively spliced mRNAs each of which encode a distince protein isoform. The product(s) of the DHDDS reaction is referred to as a polyprenolpyrophosphate. The pyrophosphate is removed by an as yet uncharacterized enzyme activity that may be either a polyprenol pyrophosphate phosphatase or a polyprenol phosphatase resulting in the formation of a polyprenol.

Steroid biotransformation ppt

steroid biotransformation ppt

Protection against one particular research toxin (7,12-DMBA) has been noted with acute usage of 9mmol/kg calcium-D-glucarate ( 3 hours prior to and another dose 30 minutes prior to DMBA injections) which reduced tumor occurrence from 100% to 30% [7] and studies with more chronic loading have noted benefit with dietary supplementation of 75mmol/kg (of the diet, /kg bodyweight and 213mg/kg human equivalent). [1] [7] This protective effect extends beyond breast cancer and is able to attenuate skin cancer with either calcium-D-glucarate itself [22] or the main bioactive metabolite [23] (skin cancer is known to be able to be induced by DMBA [24] ) and may also extend to DMBA induced oral cancers. [25]

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