Panimun Bioral 25 mg

Indications

• Low blood volume
• Hypovolemic shock
• Burns
• Cardiopulmonary bypass

Dosage

Children: Initially 10-20 mL per kilogram. Adjust according to the patient's condition and response, using 3.5-4% solution. Use under specialist supervision to mitigate the risk of fluid overload.

Adults: Dose according to requirements, typically administered intravenously. Consult product literature for specific dosing guidance.

Mechanism of action

Gelatin acts as a plasma expander by increasing the oncotic pressure in the vascular compartment, which helps to retain fluid within the bloodstream and restore circulating blood volume. This mechanism aids in maintaining blood pressure and improving tissue perfusion.

Pharmacodynamics

Gelatin solutions increase blood volume and improve hemodynamic stability in patients experiencing hypovolemic conditions. By drawing water into the vascular space, they help to counteract the effects of low blood volume, such as hypotension and compromised organ perfusion.

Pharmacokinetics

Gelatin is administered intravenously, and its effects can be observed relatively quickly. The half-life and the metabolic clearance depend on the formulation and concentration of the solution. Gelatin is gradually metabolized by macrophages and eliminated by the renal system. Close monitoring of fluid balance is essential, particularly in patients with cardiac or renal impairment.

Contra-indications

• Severe liver disease
• History of circulatory disease
• Severe cardiac disease

Adverse effects

• Fever
• Flushing
• Nausea
• Urticaria
• Rare or very rare shock

Interactions

• Calcium salts

Precautions

• Monitor cardiovascular and respiratory function
• Correct dehydration when administering
• Administer slowly to avoid rapid rise in blood pressure and cardiac failure
• Increased capillary permeability

Pregnancy

Consult product literature for specific guidance regarding use in pregnancy.

Breast-feeding

Consult product literature for specific guidance regarding use in breastfeeding.

Storage

Store at controlled room temperature, protect from light. Refer to product-specific storage instructions.

Formulations

• 5% solution for infusion
• 20% solution for infusion
• Concentrated solution (15-25% protein)
• Isotonic solution (3.5-5% protein)

Indications

• Chronic pain management
• Opioid dependence treatment
• Opioid withdrawal management

Dosage

Children: Refer to specific clinical guidelines or consult the BNF for Children for appropriate dosing information.

Adults: Refer to specific clinical guidelines or consult the BNF for appropriate dosing information.

Mechanism of action

Buprenorphine exerts its effects by binding to the mu-opioid receptors in the central nervous system, where it acts as a partial agonist. This results in analgesia and a reduction in the perception of pain. Additionally, it has antagonist properties at the kappa-opioid receptors, which may contribute to its unique profile in treating opioid addiction and dependence.

Pharmacodynamics

Buprenorphine demonstrates a dose-dependent analgesic effect and has a long duration of action due to its high affinity for opioid receptors. The partial agonist nature of buprenorphine means that it can effectively alleviate pain while minimizing the risk of overdose compared to full agonists. Its antagonist properties also play a role in preventing withdrawal symptoms in individuals with opioid dependence.

Pharmacokinetics

Buprenorphine is well absorbed after sublingual administration, with bioavailability ranging from 30% to 50%. It undergoes extensive first-pass metabolism in the liver, primarily by cytochrome P450 enzymes. The elimination half-life is variable, typically between 24 to 60 hours, allowing for once-daily dosing in maintenance therapy. It is primarily excreted in the urine as metabolites.

Pregnancy

The safety of byco during pregnancy has not been established. It is advised to weigh the potential benefits against the risks before prescribing.

Breast-feeding

It is unknown if byco is excreted in human milk. Caution is advised when administering to breastfeeding mothers.

Storage

Store at room temperature, away from light and moisture. Keep out of reach of children.

Indications

• Constipation
• Bowel preparation prior to medical examinations
• As a stimulant laxative in certain clinical situations

Dosage

Children: Refer to the BNF for Children for specific dosing information.

Adults: Refer to the BNF for specific dosing information.

Mechanism of action

Castor oil's active component, ricinoleic acid, acts as a laxative by stimulating the smooth muscles of the intestine, increasing peristalsis. It also inhibits the absorption of water from the intestinal contents, leading to increased fluid retention in the intestines, which softens the stool and promotes bowel movement.

Pharmacodynamics

The pharmacodynamic effects of castor oil include its ability to enhance gastrointestinal motility. The stimulation of the intestines is mediated through the activation of specific receptors that promote contractions of the intestinal walls. This results in a rapid laxative effect, typically within 2 to 6 hours after oral administration. Castor oil may also exert some anti-inflammatory effects, although this is less well-defined.

Pharmacokinetics

When taken orally, castor oil is absorbed in the intestines and metabolized to ricinoleic acid, which is the primary active metabolite. The onset of action usually occurs within a few hours, with the peak effect seen shortly after. The elimination half-life of castor oil is not well-established, but its effects are transient, typically lasting for several hours. Castor oil is primarily excreted in the feces, with minimal systemic absorption of the active components.

Pregnancy

Safety during pregnancy has not been established. Use only if clearly needed and if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether this drug is excreted in human milk. Caution should be exercised when administering to nursing mothers.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Indications

• Prevention of organ transplant rejection
• Management of autoimmune diseases such as rheumatoid arthritis
• Treatment of psoriasis
• Management of atopic dermatitis

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines in paediatric patients.

Adults: Refer to the BNF for specific dosing information based on the condition being treated, as doses may vary significantly.

Mechanism of action

Cyclosporine is a calcineurin inhibitor that binds to cyclophilin-1 inside cells to form a cyclosporine-cyclophilin complex. This complex inhibits calcineurin, preventing the dephosphorylation and activation of the nuclear factor of activated T cells (NF-AT). As a result, the production of cytokines such as IL-2, which is critical for T cell activation and proliferation, is suppressed. This mechanism underlies cyclosporine's immunosuppressive properties, making it effective against transplant rejection and certain autoimmune conditions.

Pharmacodynamics

Cyclosporine has potent immunosuppressive properties, particularly affecting T cells. It plays a critical role in prolonging survival after organ and bone marrow transplants by preventing and controlling serious immune-mediated reactions, such as allograft rejection and graft versus host disease. Common side effects include hypertrichosis, gingival hyperplasia, and hyperlipidemia, while nephrotoxicity is a potential concern associated with its use.

Pharmacokinetics

Cyclosporine is absorbed well from the gastrointestinal tract, although its bioavailability can be variable. It is extensively metabolized in the liver by cytochrome P450 enzymes, primarily CYP3A4. The drug is primarily excreted in the bile and has a half-life that can vary significantly among individuals. Therapeutic drug monitoring is often necessary to ensure effective and safe dosing.

Contra-indications

• Hypersensitivity to cyclosporine or any of its components
• Uncontrolled infections
• Malignancies
• Severe renal impairment
• Concurrent use with certain immunosuppressants

Adverse effects

• Nephrotoxicity
• Hypertension
• Hyperlipidemia
• Gingival hyperplasia
• Hypertrichosis
• Increased risk of infections
• Tremors
• Headaches
• Nausea
• Diarrhea

Interactions

• Other immunosuppressants may increase toxicity
• CYP3A4 inducers or inhibitors can alter cyclosporine levels
• Nonsteroidal anti-inflammatory drugs (NSAIDs) may increase nephrotoxicity
• Antifungal agents may increase cyclosporine levels
• Anticonvulsants may decrease cyclosporine levels

Precautions

• Monitor renal function regularly during treatment
• Monitor blood pressure regularly
• Assess for signs of infection
• Consider potential interactions with other medications
• Use caution in patients with a history of malignancies

Pregnancy

Cyclosporine is classified as category C. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Cyclosporine is excreted in breast milk. Caution should be exercised when administering to a nursing mother.

Storage

Store in a cool, dry place at room temperature, protected from light. Keep out of reach of children.

Formulations

• Capsules
• Oral solution
• Injection

Indications

• Iron deficiency anemia
• Chronic blood loss
• Nutritional iron deficiency
• Pregnancy-related anemia

Dosage

Children: Refer to the BNF for Children for specific dosing information as it may vary based on the formulation and clinical context.

Adults: Refer to the BNF for specific dosing information as it may vary based on the formulation and clinical context.

Mechanism of action

Ferric ions participate in various biological processes, including oxygen transport and electron transfer. They facilitate the formation of hemoglobin in red blood cells, allowing for efficient oxygen delivery throughout the body. Ferric compounds can also promote the absorption of iron from the gastrointestinal tract by providing a more bioavailable form of iron.

Pharmacodynamics

Ferric compounds exhibit their effects primarily through the restoration of iron levels in the body. This leads to improved synthesis of hemoglobin and overall enhancement of oxygen-carrying capacity. The pharmacological action is dose-dependent, with higher doses leading to more pronounced effects on hemoglobin levels and erythropoiesis. Additionally, ferric ions can influence various metabolic pathways involved in cellular respiration and energy production.

Pharmacokinetics

Ferric is absorbed in the gastrointestinal tract, with absorption rates influenced by dietary factors and the presence of other substances in the gut. Once absorbed, ferric ions are transported in the bloodstream bound to transferrin, a transport protein. The body regulates iron levels primarily through absorption rather than excretion, and excess iron can be stored in the liver, spleen, and bone marrow. The elimination of ferric compounds is generally slow, as they are incorporated into various biological systems or stored for future use.

Contra-indications

• Hypersensitivity to ferric compounds
• Iron overload conditions such as haemochromatosis or haemosiderosis
• Chronic liver disease
• Active peptic ulcer disease

Adverse effects

• Gastrointestinal disturbances including nausea, vomiting, and constipation
• Diarrhea
• Abdominal pain
• Black stools
• Allergic reactions including rashes and anaphylaxis
• Staining of teeth (with oral formulations)

Interactions

• Antacids may reduce the absorption of oral ferric preparations
• Tetracyclines and quinolone antibiotics may have reduced absorption when taken with iron
• Ascorbic acid may enhance the absorption of iron

Precautions

• Caution in patients with a history of gastrointestinal disease
• Monitor for signs of iron overload in patients receiving repeated doses
• Use with caution in patients with renal impairment

Pregnancy

Ferric compounds are generally considered safe in pregnancy when used as directed to treat iron deficiency, but should be used under medical supervision.

Breast-feeding

Ferric compounds are excreted in breast milk in small amounts, usually considered safe but should be used under medical supervision.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Oral tablets
• Oral solution
• Intravenous injection

Dosage

Children: Refer to the BNF for Children for appropriate dosing information in paediatric cases, especially in instances of overdose.

Adults: Refer to the BNF for specific dosing information based on clinical circumstances, particularly in cases of overdose.

Mechanism of action

Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is subsequently converted to glycolic, glyoxylic, and oxalic acids. These metabolites contribute to anion gap metabolic acidosis and are responsible for tissue injury through the formation of insoluble calcium oxalate crystals.

Pharmacodynamics

The toxicity of ethylene glycol arises from its metabolites, particularly glycolic and oxalic acids. These compounds induce metabolic acidosis, lead to renal failure through calcium oxalate crystal deposition in the kidneys, and can cause neurological impairment. The anion gap increases due to the accumulation of these acids, leading to complications such as cardiovascular instability and potential multi-organ failure.

Pharmacokinetics

Ethylene glycol is rapidly absorbed after oral ingestion. It undergoes first-pass metabolism primarily in the liver, where it is converted into its toxic metabolites. The elimination half-life of ethylene glycol varies but is generally prolonged in cases of renal impairment. Renal excretion of metabolites contributes to the duration of toxicity, necessitating prompt medical intervention in cases of overdose.

Adverse effects

• Metabolic acidosis
• Renal failure
• CNS depression
• Hypocalcemia
• Cardiovascular collapse
• Pulmonary edema

Precautions

• Use with caution in patients with renal impairment
• Monitor for signs of metabolic acidosis
• Evaluate electrolyte levels, particularly calcium

Pregnancy

There is limited data on the safety of ethylene glycol in pregnancy. It should only be used if clearly needed.

Breast-feeding

It is unknown if ethylene glycol is excreted in human milk. Caution is advised.

Storage

Store in a tightly closed container at room temperature, away from heat and moisture.

Formulations

• Liquid

Dosage

Children: Paediatric dosing information is not standardized and should be derived from specific product guidelines or expert consultation.

Adults: Dosage and usage depend on the specific hydrogenated compound and its intended therapeutic application. Refer to specific product guidelines for detailed dosing information.

Mechanism of action

Hydrogenation alters the molecular structure of fatty acids, transforming double bonds into single bonds. This process increases the saturation level of fats, which can influence their metabolic pathways and lipid profiles in the body.

Pharmacodynamics

The pharmacodynamic effects of hydrogenated compounds depend on the specific substance being hydrogenated. Generally, hydrogenated fats can affect lipid metabolism, potentially leading to increased levels of LDL cholesterol and decreased levels of HDL cholesterol when consumed in excess. The physiological effects may include changes in insulin sensitivity and inflammatory responses.

Pharmacokinetics

The pharmacokinetics of hydrogenated compounds vary widely based on the specific hydrogenated product. Generally, these compounds are absorbed in the gastrointestinal tract, where they may undergo further metabolism by enzymes. The bioavailability, distribution, metabolism, and excretion depend on the fatty acid composition and the presence of other dietary components.

Pregnancy

Hydrogenated compounds, depending on their specific type, may have varying safety profiles in pregnancy. It is essential to consult specific guidelines or studies related to the particular hydrogenated substance in question.

Breast-feeding

The safety of hydrogenated compounds during breastfeeding may vary. Consultation with healthcare professionals regarding specific substances is advisable.

Storage

Hydrogenated substances should be stored in a cool, dry place, away from direct sunlight and heat to maintain stability.

Indications

• Use as a sugar substitute in food products
• Suitable for diabetic patients or those on low-calorie diets
• Used in the production of sugar-free products

Dosage

Children: Refer to specific product labels for appropriate usage as maltitol is used primarily as a food additive.

Adults: Refer to specific product labels for appropriate usage as maltitol is used primarily as a food additive.

Mechanism of action

Maltitol is not fully absorbed in the gastrointestinal tract, which leads to a lower caloric intake compared to regular sugars. It is metabolized by fermentation in the colon, which may lead to the production of short-chain fatty acids that can be utilized for energy. This mechanism contributes to its reduced impact on blood glucose levels.

Pharmacodynamics

Maltitol's pharmacodynamics are characterized by its ability to provide sweetness without significantly raising blood sugar levels. It has a lower caloric value than sucrose, providing about 2.1 calories per gram compared to 4 calories per gram for sugar. Its effects on insulin response are minimal, making it suitable for individuals managing diabetes.

Pharmacokinetics

Maltitol is partially absorbed in the small intestine, with about 50-60% of the ingested amount being absorbed. The unabsorbed portion is fermented in the large intestine, which can lead to gastrointestinal side effects such as bloating and diarrhea in some individuals. The absorption rate varies among individuals, with some experiencing a higher tolerance than others.

Adverse effects

• Gastrointestinal discomfort
• Diarrhea
• Flatulence
• Abdominal pain

Precautions

• Use with caution in patients with irritable bowel syndrome
• May cause laxative effects in excessive doses
• Monitor for gastrointestinal symptoms in patients with a history of digestive disorders

Pregnancy

Safety during pregnancy has not been established. Use with caution and only if necessary.

Breast-feeding

Limited data available. Consult a healthcare provider before use.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Powder
• Granules
• Tablets

Indications

• Antimicrobial agent
• Support for immune function
• Gastrointestinal health
• Emulsifying agent in food products

Dosage

Children: Refer to specific product guidelines or consult a healthcare provider, as dosing can vary based on the formulation and intended use.

Adults: Refer to specific product guidelines or consult a healthcare provider, as dosing can vary based on the formulation and intended use.

Mechanism of action

Monolaurate exhibits its antimicrobial activity primarily through disruption of lipid membranes of bacteria, viruses, and fungi. Its mechanism involves the incorporation into the lipid bilayer of microbial cell membranes, leading to increased permeability and eventual cell lysis. This action makes it effective against a wide range of pathogens, including Gram-positive and Gram-negative bacteria.

Pharmacodynamics

Monolaurate has been shown to possess antiviral, antibacterial, and antifungal properties. The compound works by destabilizing the lipid membranes of pathogens, which can lead to their death. Additionally, it may enhance the immune response by promoting the activity of immune cells, although the exact pathways involved are still being explored. The effects of monolaurate can vary based on the concentration used and the specific microorganisms targeted.

Pharmacokinetics

Monolaurate is absorbed in the gastrointestinal tract and is rapidly metabolized into free fatty acids and glycerol. The medium-chain fatty acids can be readily transported to the liver and utilized for energy or converted into ketone bodies. Its bioavailability can be influenced by dietary fats present in the meal, as fats can enhance the absorption of monolaurate. The elimination half-life and specific metabolic pathways in humans are not well characterized, necessitating further research.

Pregnancy

There is insufficient data to determine the safety of monolaurate during pregnancy. Caution is advised.

Breast-feeding

Limited information is available on the safety of monolaurate during breastfeeding. Consult a healthcare provider before use.

Storage

Store in a cool, dry place, away from direct sunlight and heat.

Formulations

• Capsules
• Powder
• Liquid

Mechanism of action

Oxides do not have a single mechanism of action as they are a broad category of compounds. However, in general, metal oxides can exhibit catalytic properties, while non-metal oxides may participate in biochemical reactions by forming acids or bases upon dissolution in water.

Pharmacodynamics

The pharmacodynamics of oxides depend on the specific type of oxide and its interaction with biological systems. For instance, metal oxides may have antimicrobial properties, while certain non-metal oxides can influence metabolic pathways through their acid-base chemistry. The effects vary widely, necessitating specific studies for each oxide's role in therapeutic contexts.

Pharmacokinetics

The pharmacokinetics of oxides are also variable. Many metal oxides are poorly soluble and thus have limited absorption when ingested. Non-metal oxides, such as carbon dioxide, can be readily absorbed and utilized in metabolic processes. The distribution, metabolism, and excretion of oxides depend on their chemical form and the biological system in which they are involved.

Pregnancy

Not applicable as oxide is not a drug but a class of chemical compounds.

Breast-feeding

Not applicable as oxide is not a drug but a class of chemical compounds.

Storage

Store in a cool, dry place away from direct sunlight.

Indications

• Constipation
• Bowel preparation before colonoscopy or surgery

Dosage

Children: Refer to specific product guidelines for dosing instructions.

Adults: Refer to specific product guidelines for dosing instructions.

Mechanism of action

Polyoxyl works by retaining water in the stool, increasing its bulk and consistency. This osmotic effect stimulates bowel movements by softening the stool and promoting peristalsis. The water-retaining properties are attributed to its high molecular weight and hydrophilicity, which allow it to attract and hold water within the gastrointestinal tract.

Pharmacodynamics

The pharmacodynamic profile of polyoxyl includes its ability to enhance stool water content, thereby improving fecal passage through the intestines. This results in increased stool frequency and decreased transit time. Polyoxyl does not significantly affect electrolyte balance, making it a safe option for chronic constipation management.

Pharmacokinetics

Polyoxyl is not absorbed systemically; it remains in the gastrointestinal tract where it exerts its effects. The onset of action can vary but typically occurs within 24 to 72 hours after administration. The elimination of polyoxyl occurs through fecal excretion, with no significant metabolism or renal clearance involved.

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Abdominal cramps
• Allergic reactions

Precautions

• Use with caution in patients with gastrointestinal disorders.
• Monitor for allergic reactions in patients with a history of hypersensitivity.

Pregnancy

Polyoxyl is generally regarded as safe for use during pregnancy, but specific clinical guidance should be consulted.

Breast-feeding

Polyoxyl is considered safe during breastfeeding, though maternal factors should be assessed.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Formulations

• Oral solution
• Tablet
• Topical cream

Indications

• Plant growth regulation
• Agricultural applications as a growth inhibitor

Dosage

Children: Not applicable.

Adults: Refer to the relevant agricultural guidelines for specific applications.

Mechanism of action

In an in vitro study, propylene acts as a plant growth inhibitor by inhibiting the oxidation of indole-3-acetic acid by peroxidase in the presence of superoxide anion radicals. This inhibition is linked to the activation of an iron complex (compound III) shuttle, which enhances the reaction rate between superoxide and peroxidase, ultimately affecting plant growth processes. Propylene is a less effective inhibitor compared to ethylene.

Pharmacodynamics

The pharmacodynamic effects of propylene are primarily observed in its role as a growth inhibitor in plants. By modulating the oxidation of phytohormones like indole-3-acetic acid, propylene can influence various growth responses in plants, potentially affecting processes such as cell elongation and division.

Pharmacokinetics

Information on the pharmacokinetics of propylene in humans is not well-documented, as its primary uses are industrial and agricultural. Its metabolism may be influenced by environmental factors, and its effects are primarily studied in the context of plant biology rather than human pharmacology.

Mechanism of action

Cyclosporine is a calcineurin inhibitor that inhibits T cell activation. Its binding to the receptor cyclophilin-1 inside cells produces a complex known as cyclosporine-cyclophilin. This complex subsequently inhibits calcineurin, which in turn stops the dephosphorylation as well as the activation of the nuclear factor of activated T cells (NF-AT) that normally cause inflammatory reactions. NF-AT is a transcription factor that promotes the production of cytokines such as IL-2, IL-4, interferon-gamma and TNF-alpha, all of which are involved in the inflammatory process. Specifically, the inhibition of IL-2, which is necessary for T cell activation or proliferation, is believed to be responsible for cyclosporine's immunosuppressive actions. In addition to the above, the inhibition of NF-AT leads to lower levels of other factors associated with T helper cell function and thymocyte development. Cyclosporine suppresses some humoral immunity but is more effective against T cell-dependent immune mechanisms such as those underlying transplant rejection & some forms of autoimmunity. It preferentially inhibits antigen-triggered signal transduction in T lymphocytes, blunting expression of many lymphokines, including /(interleukin-2)/ IL-2, as well as expression of antiapoptotic proteins. Cyclosporine forms a complex with cyclophilin, a cytoplasmic receptor protein present in target cells. This complex binds to calcineurin, inhibiting Ca2+ stimulated dephosphorylation of the cytosolic component of NFAT. When the cytoplasmic component of NFAT is dephosphorylated, it translocates to the nucleus, where it complexes with nuclear components required for complete T-cell activation, including transactivation of IL-2 & other lymphokine genes. Calcineurin enzymatic activity is inhibited following physical interaction with the cyclosporine/cyclophilin complex. This results in the blockade of NFAT dephosphorylation; thus, the cytoplasmic component of NFAT does not enter the nucleus, gene transcription is not activated, & the T lymphocyte fails to respond to specific antigenic stimulation Cyclosporine also increases expression of transforming growth fact /beta/ (TGF-B), a potent inhibitor of IL-2-stimulated T-cell proliferation & generation of cytotoxic T lymphocytes (CTL). The exact mechanism of action is unknown but seems to be related to the inhibition of production and release of interleukin-2, which is a proliferative factor necessary for the induction of cytotoxic T lymphocytes in response to alloantigenic challenge, and which plays a major role in both cellular and humoral immune responses. Cyclosporine does not affect the nonspecific defense system of the most and does not cause significant myelosuppression. The major pharmacodynamic action of cyclosporin within T cells is calcineurin inhibition. The complex cyclophilin-cyclosporin competitively binds to the Ca(2+)- & calmodulin-dependent phosphatase calcineurin which then inhibits downstream dephosphorylation & activation of NFAT(transcription factor). The greatest calcineurin inhibition is seen 1-2 hr after admin of Neoral in parallel to the highest blood concn. Treatment of patients after organ transplantation with the immunosuppressive drug cyclosporin A (CsA) is often accompanied by impaired glucose tolerance, thus promoting the development of diabetes mellitus. ... /The authors/ show that 2-5 microM CsA diminishes glucose-induced insulin secretion of isolated mouse pancreatic islets in vitro by inhibiting glucose-stimulated oscillations of the cytoplasmic free-Ca(2+) concn [Ca(2+)](c). This effect is not due to an inhibition of calcineurin, which mediates the immunosuppressive effect of CsA, because other calcineurin inhibitors, deltamethrin & tacrolimus, did not affect the oscillations in [Ca(2+)](c) of the B-cells. The CsA-induced decr in [Ca(2+)](c) to basal values was not caused by a direct inhibition of L-type Ca(2+) channels. CsA is known to be a potent inhibitor of the mitochondr

Pharmacodynamics

Cyclosporine exerts potent immunosuppressive actions on T cells, thereby prolonging survival following organ and bone marrow transplants. This drug prevents and controls serious immune-mediated reactions including allograft rejection, graft versus host disease, and inflammatory autoimmune disease. Some notable effects of cyclosporine are hypertrichosis, gingival hyperplasia, and hyperlipidemia. There is also some debate about this drug causing nephrotoxicity.

Mechanism of action

Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is then metabolized to glycolic, glyoxylic, and oxalic acids. These acids, along with excess lactic acid are responsible for the anion gap metabolic acidosis. Oxalic acid readily precipitates with calcium to form insoluble calcium oxalate crystals. Tissue injury is caused by widespread deposition of oxalate crystals and the toxic effects of glycolic and glyoxylic acids.

Mechanism of action

In an in vitro study of the mechanism of action of ethylene as a plant growth inhibitor, the effects of ethylene and some of its analogs, including propylene, on the oxidation of indole-3-acetic acid were examined. Ethylene and its analogs inhibited the oxidation of indole-3-acetic acid by peroxidase under conditions where the iron complex (compound III, an oxy-ferrous complex of peroxidase) shuttle was activated. Inhibition occurred only in the presence of the superoxide anion radical 02(-). Spectral and kinetic data indicated that ethylene and its analogs enhanced the rate of reaction of 02(-) with peroxidase; ie, the iron complex (compound III) shuttle, resulting in the formation of compound III. Propylene was a less effective inhibitor than ethylene.