Int J Radiat Oncol Biol Phys. 1984 Dec;10:2335.
In vivo radioprotective activities of diethyldithiocarbamate (DDC).
Milas L, et al
Studies were performed to determine whether diethyldithiocarbamate protects against radiation damage to ….., hair follicles, tissues in the leg responsible for leg contractures, and a fibrosarcoma (FSA) of C3Hf/Kam mice. In most experiments,…..A dose of 400 mg/kg DDC was less effective. Protection was also significant against hair loss and leg contractures ….Therefore, DDC protected both normal tissues and FSA, but the degree of protection varied greatly. A therapeutic gain was achieved in some instances.
Edited for hair loss blog use
Int J Radiat Oncol Biol Phys. 1984 Dec;10:2335.
In vivo radioprotective activities of diethyldithiocarbamate (DDC).
Milas L, et al
Studies were performed to determine whether diethyldithiocarbamate protects against radiation damage to ….., hair follicles, tissues in the leg responsible for leg contractures, and a fibrosarcoma (FSA) of C3Hf/Kam mice. In most experiments,…..A dose of 400 mg/kg DDC was less effective. Protection was also significant against hair loss and leg contractures ….Therefore, DDC protected both normal tissues and FSA, but the degree of protection varied greatly. A therapeutic gain was achieved in some instances.
Edited for hair loss blog use
Table I summarizes the results of immunohistochemical staining of activated caspases 1-10, usurpin and XIAP in normal human hair from the scalp. Tables II and III summarize the results of positive immunoreactivity for men with AGA affected scalp and the same men 6 months after finasteride treatment, respectively. Histological analysis reveals that caspases 1, 3, 8 and 9 are all detected predominately within the isthmic and upper portion of the hair shaft in both normal and AGA patients. All specimens, whether normal or hair loss affected, as well as treated specimens, exhibit the same caspases, however, the levels of expression differ between the groups. In pattern hair loss affected tissues, the expression of caspase 1, 3, 8 and 9 is greater then normal, and after 6 months of finasteride treatment, the expression of caspases decreases, similar to the level found in normal scalp.
This is Dr Proctor’s paper on the relationship between uric acid and stroke. many of the same processes that happen in hair loss also figure in stroke causation. Similarly, many agetns that are effective in hair loss treatment are also efrfective in experimental models of stroke.
Hair loss in a blue Doberman pinscher
Color dilution alopecia, or color mutant alopecia, is an uncommon genetic-based skin disease with delayed onset (3); it has been described in many canine breeds and is more prevalent in color dilute individuals, especially those with a fawn (a dilution of a normally red or brown coat) or blue (a dilution of the normal black and tan color) coat (3). snip… The pathogenetic mechanisms of hair loss are not clearly understood. snip.. The onset of hair loss usually begins between 4 and 18 mo of age…. The condition is progressive with a gradual onset of dry, dull, and poor hair coat (6,9). Hair shafts are brittle and broken, especially along the dorsal midline (6). After several years, hypotrichosis is evident and can progress until a complete alopecia extends from the trunk to the flanks, usually sparing the head, tail, and limbs and all nondiluted coat areas. snip…Diagnosis of CDA is based on ruling out any inflammatory causes of alopecia (demodicosis, bacterial folliculitis, and dermatophytosis) and the common noninflammatory causes of alopecia, such as hypothyroidism and hyperadrenocorticis. The primary differential diagnosis for CDA is black hair follicular dysplasia (6,9), which is virtually identical histopathologically with CDA, but tan areas are spared in CDA, whereas only black areas are affected in black hair follicular dysplasia (6)….Hair examination of dogs with CDA will typically show numerous large melanin aggregates (macromelanosomes) in the hair cortex and medulla, distortion and breakage of the hair cortex, and fractures of the hair cuticle (3), as was detected in this case. Histological analysis indicates epidermal and follicular hyperkeratosis with most of the hair follicles dilated and filled with large melanin clumps. Abnormal clumping of melanin is also observed in the epidermis, dermis, and epithelia of hair follicles and around hair bulbs (6). Free melanin deposits are present at every level of the hair follicle and shaft, often with numerous perifollicular and peribulbar melanophages and pigmentary incontinence. It has been suggested that matrix hair cells are damaged by the cytotoxic effects of melanin precursor, which initiates the hair follicle dysplasia seen in the microscopic lesions and contributes to the development of the alopecia. Presence of subcuticular and intramedullary vacuoles that deform hair structure and contain melanosomes, as seen by transmission electron microscopy, may also explain hair fragility and ease of rupture and might be responsible for liberation of the melanin clumps that are released into hair follicles. There is no specific or curative therapy for color dilution alopecia (6). The vital prognosis is good, but it is preferable to prevent affected animals from breeding. Frequent baths, given once or twice/wk, with keratomodulating/antiseborrhoeic agents (benzoyl peroxide, salicylic acid, or ethyl lactate) can control the recurrence of bacterial infections, encourage restoration of normal keratinocyte multiplication, and inhibit or reduce the formation of comedones and sebum production (6). We administered oral melatonin supplementation to encourage hair regrowth, but it did not have a beneficial
Can Vet J. 2009;50: 511
effect. ..To the authors’ knowledge, there are no reports of melatonin treatment in dogs with color mutant alopecia, but oral or topical melatonin has been used to treat various other forms of canine alopecia with variable success. The mechanism by which melatonin may result in hair regrowth is not known. Melatonin is thought to play either a direct (on hair follicles) or an indirect role (within the central nervous system to alter secretion of melanocyte-stimulating hormone or prolactin secretion, or both) in the control of moulting and hair growth in mammals (2,10), but knowledge of this process is still very incomplete. It was originally hypothesized that melatonin exerted its effect on hair growth through modulating sex hormone and adrenal steroid hormone concentrations; however, decreases in hormone concentrations were not associated with hair regrowth in neutered dogs with alopecia X (1). In a recent study, it was theorized that melatonin may cause hair regrowth in dogs with hair cycle arrest by down-regulating the expression of estrogen receptors, which seem to have a role in the regulation of the anagen and telogen phases of hair (1). There are many potential reasons for failure of the treatment of the dog in our study. First, there are reports about the possible mechanisms of action, bioavailability, dosages, and seasonal/daily timing of melatonin administration, which made it difficult to determine a correct method of administration. We chose to follow the general directions given by Paradis. Additionally, because melatonin is classified as a nutraceutical, there is lack of standardization of the product, which may result in an inconsistent drug content in the final preparation. Finally, the real mechanism for development of color mutant alopecia is unknown; therefore, treatment with melatonin simply may not be effective.