Puromycin dihydrochloride belongs to the aminonucleoside family of antibiotics and is isolated from Streptomyces alboniger. Since the partial structure of this antibiotic showed it to be a purine derivative, puromycin was assigned as its generic name. Puromycin is a broad spectrum antibiotic and antibacterial agent. It is active against Gram-positive microorganisms, less active against acid-fast bacilli, and weakly active against Gram-negative microorganisms. It acts very quickly and can kill 99% of the cells within 2 days. It also exhibits antitumor activity in studies on brain tumor cells. Puromycin is a protein synthesis inhibitor that causes premature chain termination by acting as an analog of the 3’-terminal end of aminoacyl-tRNA. It has been used to study transcriptional regulatory mechanisms that control the sequential and coordinate expression of genes during cell differentiation.

Tetrachloroethylene is a nonflammable colorless liquid. Other names for tetrachloroethylene include perchloroethylene, PCE, PERC, tetrachloroethene, and perchlor. Tetrachloroethylene is used as a dry cleaning agent and metal degreasing solvent. It is also used as a starting material (building block) for making other chemicals and is used in some consumer products. It has also been used in water repellants, paint removers, printing inks, glues, sealants, polishes, and lubricants. Tetrachloroethylene has been in commercial use since the early 1900s. Tetrachlorethylene has been suspected of causing some types of cancer, based on both human and animal evidence. Laboratory studies have found that ingesting or inhaling tetrachlorethylene increased the risk of liver cancer in mice. In rats, inhaling tetrachloethylene was linked to kidney cancer and a rare type of leukemia. EPA has classified tetrachloroethylene as likely to be carcinogenic to humans by all routes of exposurebased on suggestive evidence in epidemiological studies and conclusive evidence in rats (mononuclear cellleukemia) and mice (increased incidence of liver tumors). The International Agency for Research on Cancer(IARC) has classified tetrachloroethylene as probably carcinogenic to humans (Group 2A).

Cycloheximide is an antibiotic produced by fermentation culture of Streptomyces griseus, Streptomyces noursei, Streptomyces albulus, Streptomyces naraensis, or other cycloheximide-producing microorganism. It was first discovered by A. Whiffen et al. in 1946. She observed the activity of the compound against the yeasts and it became known as the first antifungal antibiotic. Cycloheximide has been marketed as a plant fungicide for many years and this use continues mainly against fungal diseases of turf and for powdery mildew on roses. More recently, cycloheximide has been recognized and is being developed as an abscission agent for citrus fruits and olives. Due to significant toxic side effects, including DNA damage, teratogenesis, and other reproductive effects, cycloheximide is generally used only in in vitro research applications, and is not suitable for human use as a therapeutic compound. Cycloheximide is an antimitotic and an inhibitor of the synthesis of both DNA and protein.

Epostane (WIN-32729) a pure competitive inhibitor of 3-beta-hydroxysteroid dehydrogenase. Epostane blocks progesterone synthesis during the luteal phase and in pregnancy in women and has strong anti-steroidogenic effect in endocrine tissues. Epostane is an abortifacient agent in early human pregnancy. It inhibits ovarian follicular steroidogenesis and ovulation.

Dithiothreitol is a chemical reagent with a wide actuation spectrum not only from a laboratorial view but also from a therapeutic standpoint, more clinical and practical. DTT (i) is frequently used in a variety of experiences that involve proteins or peptides, protecting sulfhydryl groups from oxidation and reducing disulfide bonds between cysteines; (ii) is also used in the study of disulfide exchange reactions of protein disulfides; (iii) is able to keep glutathione in the reduced state; (iv) acts as an "antidote" enabling the activity of detoxification systems; (v) participates in cellular mechanisms such as vesiculation, cell morphology, signal transduction pathways (hormone-'like' role), etc.; (vi) can be used in the treatment approach of diseases like cystinosis or medical conditions resulting from ion or metal toxicity. DTT is as a reducing or "deprotecting" agent. DTT protects notably enzyme activity loss by the oxidation of sulfhydryl groups. The DTT removal is performed by standard desalting.procedures (dialysis, gelfiltration). As an antioxidant, it is used as a protective agent against ionizing radiations in living cells. It has been used to enhance or inhibit enzymes or receptors activity.

Clorgiline is a monoamine oxidase (MAO) inhibitor. Specifically, it is an irreversible and selective inhibitor of MAO-A. Clorgiline was under investigation for antidepressant and anxiolytic potential but has never been marketed, likely due to efficacy concerns. It continues to see routine use as a molecular probe in biomedical research examining a number of neurological disease and cancer models. In addition to inhibiting the MAO-A receptor, it has also been found to bind to the sigma1 receptor, and with high affinity to the I2 imidazoline receptor.

Berythromycin or erythromycin B (also known as 12-deoxyerythromycin A), an acid-stable co-metabolite of the antibiotic erythromycin A, exhibits broad-spectrum antibiotic activity. The antibacterial activity of erythromycin B is similar to that of erythromycin A, but after acid-treatment, resembling exposure to the stomach, erythromycin B substantially retains antibacterial activity, whereas erythromycin A does not. Erythromycin B played an integral part of the structure activity relationship studies of semi-synthetic erythromycins.

Fusaric acid (J-butylpicolinic acid) is a fungal toxin with low to moderate toxicity synthesized by some Fusurium species which cause infections in cereal grains and other agricultural commodities. It may potentiate the effects of other Fusurium toxins. Fusaric acid is a potent inhibitor of DNA synthesis. Fusaric acid has potent anti-proliferative activity in vitro on various normal and cancer cell lines and suggest that it exhibits some cytotoxic specificity for growing and confluent colorectal adenocarcinoma and mammary adenocarcinoma cell lines. Fusaric acid is known as a potent dopamine-beta-hydroxylase inhibitor of high specificity. Fusaric acid calcium salt elicited the hypotensive response primarily through the reduction of total peripheral vascular resistance index.

Urocanic acid is a breakdown (deamination) product of histidine. In the liver, urocanic acid is an intermediate in the conversion of histidine to glutamic acid, whereas in the epidermis, it accumulates and may be both a UV protectant and an immunoregulator. Urocanic acid (UA) exists as a trans isomer (t-UA, approximately 30 mg/cm2) in the uppermost layer of the skin (stratum corneum). t-UA is formed as the cells of the second layer of skin become metabolically inactive. During this process, proteins and membranes degrade, histidine is released, and histidase (histidine ammonia lyase) catalyzes the deamination of histidine to form t-UA. t-UA accumulates in the epidermis until removal by either the monthly skin renewal cycle or sweat. Upon absorption of UV light, the naturally occurring t-UA isomerizes to its cis form, c-UA. Because DNA lesions (e. g. , pyrimidine dimers) in the lower epidermis can result from UV-B absorption, initial research proposed that t-UA acted as a natural sunscreen absorbing UV-B in the stratum corneum before the damaging rays could penetrate into lower epidermal zones. c-UA also suppresses contact hypersensitivity and delayed hypersensitivity, reduces the Langerhans cell count in the epidermis, prolongs skin-graft survival time, and affects natural killer cell activity. It has also been proposed that c-UA may mediate the transient alteration in immune surveillance resulting in immunosuppression induced after UV-irradiation, by interacting with immune cells locally and/or systemically to generate T cells with suppressor function.

Biologically, methanogens in the colon can use carbon dioxide and hydrogen to produce methane as a by-product. It was previously considered that humans do not utilize methane. However, in a recent study on rodents, results demonstrated that methane could exert anti-inflammatory, anti-oxidant and anti-apoptotic effects. Furthermore, it has bee suggested, that methane-rich saline could be a promising therapeutic agent for clinical treatment of pancreatitis. Methane gas may also be a promising option for the clinical treatment of Acute Lung Injury and Spinal Cord Injury. The exact mechanism underlying the antioxidative, anti-inflammatory, and antiapoptotic activities of methane is not obvious. Different researchers have proposed different hypotheses. Some have hypothesized that methane might accumulate transiently at the interfaces of cell membranes, thereby changing the physicochemical properties or the in-situ functionality of proteins embedded within this environment. Other investigators have suggested that methane could exert effects on membrane channels affecting G-proteins, membrane or receptor-mediated signaling, or acetylcholine-activated ion channel kinetics. It is unknown if mammalian cells contain an oxygenase that is capable of using methane as a substrate, or if the biological effects of methane are caused by the formation of small amounts of the reactive alcohol, methanol, and/or changes in the redox milieu of the cell due to changes in NAD(P)+/NAD(P)H ratio, and whether or not there is a cellular “receptor” for methane. There are also questions remaining around the difference between intraperitoneal vs inhaled administration of methane.