SULFZINC 15%W/W, 5%W/W OINTMENT

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

• Acne vulgaris
• Seborrheic dermatitis
• Scabies
• Tinea infections

Dosage

Children: Refer to the BNF for Children for specific dosing guidelines tailored for pediatric patients.

Adults: Refer to the BNF for specific dosing guidelines based on the formulation and condition being treated.

Mechanism of action

Topically applied sulfur exhibits mild antifungal and antibacterial activity. It is suggested that sulfur forms hydrogen sulfide and/or polythionic acid, which may exert germicidal effects. The antifungal activity is largely attributed to its keratolytic action, leading to the shedding of fungal spores and hyphae within the stratum corneum. It has shown potent inhibitory effects against some streptococci and moderate effects against Staphylococcus aureus, while showing no activity against gram-negative bacteria. Its antibacterial action may result from the inactivation of sulfhydryl groups in bacterial enzyme systems. Additionally, sulfur is toxic to the parasitic arthropod Sarcoptes scabiei, further supporting its use in treating scabies.

Pharmacodynamics

Sulfur's pharmacodynamic effects are mainly due to its ability to promote keratolysis, allowing for the removal of dead skin cells and facilitating the treatment of acne and other skin conditions. Its antibacterial properties help reduce bacterial load on the skin, which is essential for preventing infection and controlling acne lesions. The exact mechanisms for its action in acne treatment are not fully elucidated but involve a combination of these effects.

Pharmacokinetics

When applied topically, sulfur is minimally absorbed systemically, which limits potential systemic side effects. Its local effects are prominent as it acts directly on the affected skin areas. The keratolytic action occurs relatively quickly, while the antimicrobial effects may vary based on the microbial strain and concentration used.

Adverse effects

• Skin irritation
• Dryness
• Redness
• Peeling
• Allergic reactions

Precautions

• Use with caution in patients with sensitive skin
• Avoid contact with eyes and mucous membranes

Pregnancy

Use during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Use with caution while breastfeeding, as it is not known whether sulfur is excreted in human milk.

Storage

Store in a cool, dry place away from light.

Formulations

• Topical cream
• Topical lotion
• Topical ointment

Mechanism of action

Topically applied sulfur has mild antifungal and antibacterial activity. It has been suggested that when applied topically to the skin, sulfur forms hydrogen sulfide and/or polythionic acid, which may exert germicidal activity. In vitro studies indicate that sulfur has little if any fungistatic or fungicidal activity. Therefore, sulfur's antifungal activity probably results largely from its keratolytic action, causing shedding of fungal spores and hyphae embedded within the stratum corneum. In vitro, sulfur has been shown to have some antibacterial activity; the drug has a potent inhibitory effect against some streptococci, a moderate inhibitory effect against Staphylococcus aureus, and no activity against gram-negative bacteria. It has been suggested that the drug's antibacterial activity may partly result from inactivation of sulfhydryl groups contained in bacterial enzyme systems, since the antibacterial effect of the drug has reportedly been neutralized by addition of cysteine and other sulfhydryl-containing compounds to the culture medium. Topically applied sulfur is reportedly toxic to the parasitic arthropod Sarcoptes scabiei. The exact mechanism(s) of action of "sulfur" in the treatment of acne is not fully understood but is presumed to involve the drug's keratolytic and antibacterial effects. Although some studies indicate that "sulfur" may also be comedogenic, other studies have been unable to substantiate this effect and the drug generally is considered effective in the topical treatment of acne. The aim of this research was to analyze the effects and the modes of action of elemental sulfur (S(0)) in bioluminescence and respiration of Vibrio fischeri cells and the enzymes crude luciferase, pure catalase, and alcohol dehydrogenase (ADH). Metallic copper removed sulfur and reduced the toxicity of acetone extracts of sediment samples analyzed in the bioluminescence test. The sulfur inhibition of cell bioluminescence was noncompetitive with decanal, the luciferase substrate; reversible, with maximum toxicity after 15 min (EC50 = 11.8 ug/L); and almost totally recovered after 2 hr. In vitro preincubation of crude luciferase extract with sulfur (0.28 ppm) weakly inhibited bioluminescence at 5 min, but at 30 min the inhibition reached 60%. Increasing the concentration of sulfur in the parts per million concentration range in vitro decreased bioluminescence, which was not constant, but depended on exposure time, and no dead-end/total inhibition was observed. The redox state of enzymes in the in vitro system significantly affected inhibition. Hydrogen peroxide restored fully and the reducing agent dithiothreitol, itself toxic, restored only partially luciferase activity in the presence of sulfur. Sulfur (5.5 ppm) slightly inhibited ADH and catalase, and dithiothreitol enhanced sulfur inhibition. High sulfur concentrations (2.2 ppm) inhibited the bioluminescence and enhanced the respiration rate of V. fischeri cells. Elemental sulfur data were interpreted to show that sulfur acted on at least a few V. fischeri cell sites: reversibly modifying luciferase at sites sensitive to/protected by oxidative and reducing agents and by affecting electron transport processes, resulting in enhanced oxygen consumption. Sulfur together with an enzyme reducing agent inhibited the oxidoreductive enzymes ADH and catalase, which have /thiol/ groups, metal ion cofactors, or heme, respectively, in their active centers. Sulfur must be converted to pentathionic acid (H2S5O6) in order to exert germicidal action. Presumably oxidation of sulfur to pentathionic acid is accomplished by certain microorganisms or by epidermal cells when element is applied to skin. Sulfur possesses a keratolytic property, which may be the basis for the therapeutic action of the element in certain cutaneous disorders unassociated with infection.