Categories
Toxicology

Given what we’ve read about alcohol and its effects on the body and subsequent medical problems, why do you think alcohol is considered different from other drugs in our society?

Given what we’ve read about alcohol and its effects on the body and subsequent medical problems, why do you think alcohol is considered different from other drugs in our society?
How is alcohol different from marijuana, cocaine, heroin, MDMA or any other drug of abuse?
Do you think society effectively educates people about alcohol use/abuse/dependence?
How would you go about educating society about alcohol?

Categories
Toxicology

The quantitative conclusion from this study was that 3000 mg re/day of supplemental vitamin a can be considered as a threshold for teratogenicity, which would be associated with a low or negligible risk of teratogenicity (scf, 2002).teratogenicity :

Acute toxicity:
55 male and 55 female Sprague-Dawley rats were administered does orally at levels of 3160–8250 mg/kg bw. Body weights were determined on regular intervals and animal were observed on regular intervals for treatment related effects, including mortality. Calculated acute oral LD50 for retinyl acetate corresponded to 15.4 mio IU/kg bw in males, 13.9 mio IU/kg bw in females and 14.5 mio IU/kg bw combined, respectively. SCCS 2016 confidential data.
The SCCS ranked the acute oral toxicity of the three retinoids as the following: retinol > retinyl acetate > retinyl palmitate.
Repeated dose toxicity:
Numerous safety studies on different species including mice, rats, rabbits, dogs, guinea
pigs, cattle, chicken, pigs, ducks, hamsters, monkeys, sheep and cats have been performed
to investigate the toxicity of Vitamin A. In these studies Vitamin A and its metabolites were
tested via oral, intravenous, intramuscular, subcutaneous, intraperitoneal and dermal
administration routes. The toxicity of Vitamin A was also assessed by several regulatory or
expert bodies: e.g. EFSA (2006, 2015), EMEA (2015), CIR (2013), COT (2013), BfR (2012),
VKM (2012), ANSM (2010), SCF 2002. Toxicity appears to occur when the amount of
vitamin A in plasma exceeds the capacity of Retinol Binding Proteins, leading to a change in
the ratio of free retinol to retinol-RBP complexes. Only a summary of the main points
related to the toxicity of Vitamin A that can be used to assess the risk for cosmetic exposure
is included in this section.
The teratogenic potential of Vitamin A and effects on bone were considered as the most
critical toxicological endpoints and have therefore been dealt with in more detail than other
possible adverse effects.
In 2002, the SCF reviewed possible adverse effects of long-term intake of retinol and retinyl
esters (SCF, 2002). The following adverse effects were identified: hepatotoxicity, changes in
lipid metabolism and in bone density, and teratogenicity. The lowest continuous daily
consumption in patients with cirrhosis was 7500 mg RE/day taken over 6 years. A case of
cirrhosis from 7500 mg RE/day for 6 years has been reported (Kowalski et al., 1994), in
which progressive liver failure led to the death of the patient. Cases of hepatotoxicity have
not been reported below 7500 mg RE/day, and it can be hypothesised that this value might
be the upper threshold of the storage capabilities of the liver. The SCF also identified the
daily dose of 7500 μg RE/day for four years as the LOAEL for changes in lipid metabolism,
resulting in a 2-3% increase in blood cholesterol concentration in a placebo-controlled trial
involving 2,297 63 years old subjects, which could lead to an increased risk of
cardiovascular disease. The SCF reported reduced bone density and increased rates of
fracture in women aged 40-76 years with daily intake of Vitamin A greater than 1500 μg
RE/day in comparison with intakes of less than 500 μg RE/day and commented that middle
aged and elderly women were the group most sensitive to such effects. It was not known
however, whether the same dose-response relationship would apply in men or in children.
Based on epidemiological data, no association has been found in the majority of casecontrol
studies between daily doses of Vitamin A of 3000 mg RE or less and foetal
malformation. However, in each of these studies, the number of women consuming high
amounts of Vitamin A was too limited to give a reliable estimate of a safe intake value.
A prospective study involving 22,748 pregnant women was large enough to stratify the
population according to the Vitamin A intake. Moreover, the origin of the Vitamin A intake
(supplement or food) was available for all subjects. Women taking more than 4500 mg RE
of total Vitamin A (from food and supplement) daily had a 3.5 times higher risk of giving
birth to a child with cranial-neural-crest defects, than mothers ingesting less than 1500 mg
RE/day. When the analysis was restricted to the supplemental intake of Vitamin A only, the
relative risk for mothers ingesting more than 3000 mg RE/day was 4.8 higher than those
ingesting 1500 mg RE/day. The authors fitted a regression curve to their data, which
indicated a rise in the ratio of prevalence of birth defects associated to the cranial-neural
crest at doses greater than 3000 mg RE/day of Vitamin A (food and supplement). The
conclusions of the study remained the same when several potential confounding factors
were considered. The quantitative conclusion from this study was that 3000 mg RE/day of
supplemental Vitamin A can be considered as a threshold for teratogenicity, which would be
associated with a low or negligible risk of teratogenicity (SCF, 2002).Teratogenicity :
The SCF set a Tolerable Upper Intake Level (UL) for preformed Vitamin A4 (retinol, retinal,
retinyl esters and retinoic acid) of 3000 μg RE/day (or 10 000 IU) for women of childbearing
age and men, based on the risk of teratogenicity and hepatotoxicity. This UL also applies
during pregnancy and lactation. ULs for children were extrapolated from the UL for adults,
based on allometric scaling (body weight to the power of 0.75). ULs were set at 800 μg
RE/day for children aged 1–3 years, 1 100 μg RE/day for children aged 4–6 years, 1 500 μg
RE/day for children aged 7–10 years, 2 000 μg RE/day for children aged 11–14 years and 2
600 μg RE/day for children aged 15–17 years.
In a subsequent assessment which considered studies published until 2004, the Scientific
Advisory Committee on Nutrition (SACN, 2005) concluded that the evidence of an
association between high intake of retinol and poor bone health was inconsistent. The
Committee noted that some epidemiological data suggest that a retinol intake of 1500
μg/day and above is associated with an increased risk of bone fracture; the evidence was
considered not robust enough to set a Safe Upper Level, and a Guidance Level for retinol
intake of 1 500 μg/day was set for adults for individuals at greater risk of osteoporosis and
bone fracture (particularly post-menopausal women) (EFSA, 2008, 2013).
The EFSA NDA Panel5 (EFSA, 2015) was aware that additional observational studies on possible associations between retinol and Vitamin A intake and bone health have been published since the SCF and SACN assessments. An overview of prospective cohort and nested case–control studies which investigated an association of retinol or “Vitamin A” intake with the risk of bone fracture has been performed. Based on this review, the Panel considered that evaluation of the data published since the SCF assessment does not change the conclusion from that of the SCF with respect to the association between retinol or Vitamin A intake and risk of bone fracture in postmenopausal women. In summary, the critical adverse effects of high intakes of Vitamin A are different at different stages of life, such as bulging fontanelles in infants, decreased bone density and increased bone fracture in middle aged and elderly women, and teratogenicity in women of child-bearing age. Hepatotoxicity and altered lipid metabolism are also relevant for adults. Teratogenicity:
Extensive research carried out over the last 100 years has established that vitamin A plays
crucial roles in embryonic development by regulating organogenesis, cell proliferation,
differentiation and apoptosis. Because of the importance of vitamin A during development,
the transport via the placenta is tightly regulated and it is documented that both low and
excess dietary levels of vitamin A may induce malformations in experimental animals and
humans indicating that the concentration must be within a narrow range to avoid birth defects
(SCF, 2002; Blomhoff et al., 2003; Gutierrez-Mazariegos et al., 2011).
Because vitamin A bioaccumulate in the human liver, intake of large doses in the months
before conception may lead to increased teratogenic risk. In a prospective study performed by
Rothman et al. (1995) which included 22748 pregnant women, it was concluded that intake of
more than 10000 IU (3000 μg RE) of supplemental vitamin A per day was associated with
increased risk of birth defects. In this study, 1.3% of babies born to women who took 5000 IU
(1500 μg RE) or less of vitamin A supplement had cleft lip, cleft palate, hydrocephalus or
major heart defects, while 3.2% of infants born to women who took over 10000 IU/day had
such defects (Rothman et al., 1995). One prospective study including exposures of more than
50000 (>15000 μg RE) and 100000 IU (>30000 μg RE) per day and available
epidemiological data on intake in the lower-dose ranges support the conclusion that daily
intake of 10000 IU (3000 μg RE) per day would be associated with a low or negligible risk of
teratogenicity (Mastroiacovo et al., 1999; SCF, 2002; Blomhoff et al., 2003).
Teratogenic effects after oral exposure to vitamin A in humans are best documented in
children born to mothers treated with the pharmaceutical Accutane, 13-cis-retinoic acid
(isotretionin) during pregnancy. Accutane entered the U.S. market in 1982 for the treatment of
severe acne, and already 3 years later Lammer et al. (1985) reported high risk for spontaneous
abortion, premature birth, perinatal mortality and major malformations associated with
exposure to the therapeutic dose. The pattern of malformations reflected the birth defects
observed in animal studies including craniofacial, cardiac, thymic, and CNS deformities. The
most frequently occurring category was CNS malformations (Lammer et al., 1985; 1988).
Furthermore, longitudinal follow-up of the children, both with and without major
malformations, indicated that 47% of the children had mental ability scores in the borderline
to the mentally retarded range (Adams and Lammer, 1993).
As opposed to oral intake, more than 25 years of topical use of RA for acne are without
evidence for increased teratogenicity. In a case control study of 215 mothers exposed to
tretinoin during pregnancy, the prevalence of major foetal malformations was 1.9 in the
treatment group versus 2.6 in the control group (Jick et al., 1993 cited in Mukherjee et al.,
2006). However, it is still being warned against using the drug retinoic acid during pregnancy.
Dermal absorption:
In vitro
Freshly biopsied human skin from abdominal surgery of 2 volunteers was used to test dermal permeation with either a gel or oil-in-water emulsion of 0.3% [3H]-retinol. The retinol dose (2 mg/cm² application amount) was applied to each diffusion cell for 24 h, and then washed off to remove any unabsorbed material. A fraction collector was used to collect receptor fluid as 6-h fractions for a total of 24 or 72 h. At the end of the study (24 or 72 h), the skin was removed from the diffusion cell and the amount of retinol remaining in the skin was determined. Only small amounts remained in the viable skin (epidermis/dermis) or receptor fluid. The portion penetrated into the skin of human (SC, viable skin) amounted to 5.7% or 8.9% after 24 hours with values of 3.8% and 7.8% after 72 hours for the gel or emulsion, respectively. The bioavailable portion amounted to 2.4% or 4.3% after 24 hours with values of 1.5% and 5.1% after 72 hours of the applied dose level for the gel or emulsion, respectively under the study conditions.
Freshly biopsied human skin from abdominal surgery of 3 female volunteers was placed on static diffusion cells to test dermal bioavailablity of retinyl palmitate emulsion with a content of 0.15% [14C]-retinyl palmitate ([14C]-RP) when applied for 16h. Majority the test substance was attached to the SC. Only small amounts could be detected in the remaining skin tissues and only negligible amounts in the receptor fluid. The portion penetrated into the skin (SC, epidermis, dermis) was in the range of 0.30-0.33 μg/cm² or 9.1–10.5% with respect to the applied dose. The bioavailable portion ranged between 0.033–0.036 μg/cm² corresponding to 1.1–1.24% of the applied dose level under the study conditions. In vivo
Two groups of female volunteers were treated topically for 21 days with creams containing 0.3% retinol or 0.55% retinyl palmitate on about 3000 cm2 of their body surface (back, upper legs). Daily, 3.5 g of cream was applied comprising 9 mg of retinol or 16 mg of retinyl palmitate. Plasma levels of retinol, retinyl palmitate, retinyl oleate, retinyl stearate, 9-cis-, 13-cis-, all-trans-, 13-cis-4-oxo- or all-trans-oxo-retinoic acids were measured 0, 1, 2, 4, 6, 8, 12, 14-16 and 24 hours after each application. On day 21, no changes in plasma retinoid levels were observed.

Categories
Toxicology

Given what we’ve read about alcohol and its effects on the body and subsequent medical problems, why do you think alcohol is considered different from other drugs in our society?

Given what we’ve read about alcohol and its effects on the body and subsequent medical problems, why do you think alcohol is considered different from other drugs in our society?
How is alcohol different from marijuana, cocaine, heroin, MDMA or any other drug of abuse?
Do you think society effectively educates people about alcohol use/abuse/dependence?
How would you go about educating society about alcohol?

Categories
Toxicology

Review the evidence of harm resulting from exposure to dpm, using both human and animal studies to consider the dose effect/ response relationship (at least 4 journal articles are required).

Review the evidence of harm resulting from exposure to DPM, using both human and animal studies to consider the dose effect/ response relationship (at least 4 journal articles are required). Ascertain the threshold of harm for DPM and compare this with the Occupational Exposure Limit (OEL). Discuss the differences you find with references and the appropriate literature.

Categories
Toxicology

E. pathways of elimination for dpm

Discuss the toxicology of DPM as per the following headings:
a. absorption,
b. distribution in the body and target organs,
c. pathways for biotransformation,
d. mechanisms of harm (interaction with cells and tissues)
e. pathways of elimination for DPM

Categories
Toxicology

Learning Goal: I’m working on a toxicology test / quiz prep and need an explanat

Learning Goal: I’m working on a toxicology test / quiz prep and need an explanation and answer to help me learn.A 70-year-old man had suffered from gastric carcinoma complicated with bronchopneumonia. The autopsy revealed enlarged firm liver with multiple nodular implants and acute abscesses in the kidney.
Questions
1. Describe the liver on gross inspection.
2. What is the cause of the development of this injury in the liver?
3. Describe the kidney on gross inspection.
4. What is the cause of the development of this injury in the kidney?
5. How can embolism be characterized in terms of its type?

Categories
Toxicology

The quantitative conclusion from this study was that 3000 mg re/day of supplemental vitamin a can be considered as a threshold for teratogenicity, which would be associated with a low or negligible risk of teratogenicity (scf, 2002).teratogenicity :

Learning Goal: I’m working on a toxicology exercise and need a sample publish to help me learn.
Acute toxicity:
55 male and 55 female Sprague-Dawley rats were administered does orally at levels of 3160–8250 mg/kg bw. Body weights were determined on regular intervals and animal were observed on regular intervals for treatment related effects, including mortality. Calculated acute oral LD50 for retinyl acetate corresponded to 15.4 mio IU/kg bw in males, 13.9 mio IU/kg bw in females and 14.5 mio IU/kg bw combined, respectively. SCCS 2016 confidential data.
The SCCS ranked the acute oral toxicity of the three retinoids as the following: retinol > retinyl acetate > retinyl palmitate.
Repeated dose toxicity:

Numerous safety studies on different species including mice, rats, rabbits, dogs, guinea
pigs, cattle, chicken, pigs, ducks, hamsters, monkeys, sheep and cats have been performed
to investigate the toxicity of Vitamin A. In these studies Vitamin A and its metabolites were
tested via oral, intravenous, intramuscular, subcutaneous, intraperitoneal and dermal
administration routes. The toxicity of Vitamin A was also assessed by several regulatory or
expert bodies: e.g. EFSA (2006, 2015), EMEA (2015), CIR (2013), COT (2013), BfR (2012),
VKM (2012), ANSM (2010), SCF 2002. Toxicity appears to occur when the amount of
vitamin A in plasma exceeds the capacity of Retinol Binding Proteins, leading to a change in
the ratio of free retinol to retinol-RBP complexes. Only a summary of the main points
related to the toxicity of Vitamin A that can be used to assess the risk for cosmetic exposure
is included in this section.
The teratogenic potential of Vitamin A and effects on bone were considered as the most
critical toxicological endpoints and have therefore been dealt with in more detail than other
possible adverse effects.
In 2002, the SCF reviewed possible adverse effects of long-term intake of retinol and retinyl
esters (SCF, 2002). The following adverse effects were identified: hepatotoxicity, changes in
lipid metabolism and in bone density, and teratogenicity. The lowest continuous daily
consumption in patients with cirrhosis was 7500 mg RE/day taken over 6 years. A case of
cirrhosis from 7500 mg RE/day for 6 years has been reported (Kowalski et al., 1994), in
which progressive liver failure led to the death of the patient. Cases of hepatotoxicity have
not been reported below 7500 mg RE/day, and it can be hypothesised that this value might
be the upper threshold of the storage capabilities of the liver. The SCF also identified the
daily dose of 7500 μg RE/day for four years as the LOAEL for changes in lipid metabolism,
resulting in a 2-3% increase in blood cholesterol concentration in a placebo-controlled trial
involving 2,297 63 years old subjects, which could lead to an increased risk of
cardiovascular disease. The SCF reported reduced bone density and increased rates of
fracture in women aged 40-76 years with daily intake of Vitamin A greater than 1500 μg
RE/day in comparison with intakes of less than 500 μg RE/day and commented that middle
aged and elderly women were the group most sensitive to such effects. It was not known
however, whether the same dose-response relationship would apply in men or in children.
Based on epidemiological data, no association has been found in the majority of casecontrol
studies between daily doses of Vitamin A of 3000 mg RE or less and foetal
malformation. However, in each of these studies, the number of women consuming high
amounts of Vitamin A was too limited to give a reliable estimate of a safe intake value.
A prospective study involving 22,748 pregnant women was large enough to stratify the
population according to the Vitamin A intake. Moreover, the origin of the Vitamin A intake
(supplement or food) was available for all subjects. Women taking more than 4500 mg RE
of total Vitamin A (from food and supplement) daily had a 3.5 times higher risk of giving
birth to a child with cranial-neural-crest defects, than mothers ingesting less than 1500 mg
RE/day. When the analysis was restricted to the supplemental intake of Vitamin A only, the
relative risk for mothers ingesting more than 3000 mg RE/day was 4.8 higher than those
ingesting 1500 mg RE/day. The authors fitted a regression curve to their data, which
indicated a rise in the ratio of prevalence of birth defects associated to the cranial-neural
crest at doses greater than 3000 mg RE/day of Vitamin A (food and supplement). The
conclusions of the study remained the same when several potential confounding factors
were considered. The quantitative conclusion from this study was that 3000 mg RE/day of
supplemental Vitamin A can be considered as a threshold for teratogenicity, which would be
associated with a low or negligible risk of teratogenicity (SCF, 2002).Teratogenicity :
The SCF set a Tolerable Upper Intake Level (UL) for preformed Vitamin A4 (retinol, retinal,
retinyl esters and retinoic acid) of 3000 μg RE/day (or 10 000 IU) for women of childbearing
age and men, based on the risk of teratogenicity and hepatotoxicity. This UL also applies
during pregnancy and lactation. ULs for children were extrapolated from the UL for adults,
based on allometric scaling (body weight to the power of 0.75). ULs were set at 800 μg
RE/day for children aged 1–3 years, 1 100 μg RE/day for children aged 4–6 years, 1 500 μg
RE/day for children aged 7–10 years, 2 000 μg RE/day for children aged 11–14 years and 2
600 μg RE/day for children aged 15–17 years.
In a subsequent assessment which considered studies published until 2004, the Scientific
Advisory Committee on Nutrition (SACN, 2005) concluded that the evidence of an
association between high intake of retinol and poor bone health was inconsistent. The
Committee noted that some epidemiological data suggest that a retinol intake of 1500
μg/day and above is associated with an increased risk of bone fracture; the evidence was
considered not robust enough to set a Safe Upper Level, and a Guidance Level for retinol
intake of 1 500 μg/day was set for adults for individuals at greater risk of osteoporosis and

bone fracture (particularly post-menopausal women) (EFSA, 2008, 2013).
The EFSA NDA Panel5 (EFSA, 2015) was aware that additional observational studies on possible associations between retinol and Vitamin A intake and bone health have been published since the SCF and SACN assessments. An overview of prospective cohort and nested case–control studies which investigated an association of retinol or “Vitamin A” intake with the risk of bone fracture has been performed. Based on this review, the Panel considered that evaluation of the data published since the SCF assessment does not change the conclusion from that of the SCF with respect to the association between retinol or Vitamin A intake and risk of bone fracture in postmenopausal women. In summary, the critical adverse effects of high intakes of Vitamin A are different at different stages of life, such as bulging fontanelles in infants, decreased bone density and increased bone fracture in middle aged and elderly women, and teratogenicity in women of child-bearing age. Hepatotoxicity and altered lipid metabolism are also relevant for adults.
Teratogenicity:
Extensive research carried out over the last 100 years has established that vitamin A plays
crucial roles in embryonic development by regulating organogenesis, cell proliferation,
differentiation and apoptosis. Because of the importance of vitamin A during development,
the transport via the placenta is tightly regulated and it is documented that both low and
excess dietary levels of vitamin A may induce malformations in experimental animals and
humans indicating that the concentration must be within a narrow range to avoid birth defects
(SCF, 2002; Blomhoff et al., 2003; Gutierrez-Mazariegos et al., 2011).
Because vitamin A bioaccumulate in the human liver, intake of large doses in the months
before conception may lead to increased teratogenic risk. In a prospective study performed by
Rothman et al. (1995) which included 22748 pregnant women, it was concluded that intake of
more than 10000 IU (3000 μg RE) of supplemental vitamin A per day was associated with
increased risk of birth defects. In this study, 1.3% of babies born to women who took 5000 IU
(1500 μg RE) or less of vitamin A supplement had cleft lip, cleft palate, hydrocephalus or
major heart defects, while 3.2% of infants born to women who took over 10000 IU/day had
such defects (Rothman et al., 1995). One prospective study including exposures of more than
50000 (>15000 μg RE) and 100000 IU (>30000 μg RE) per day and available
epidemiological data on intake in the lower-dose ranges support the conclusion that daily
intake of 10000 IU (3000 μg RE) per day would be associated with a low or negligible risk of
teratogenicity (Mastroiacovo et al., 1999; SCF, 2002; Blomhoff et al., 2003).
Teratogenic effects after oral exposure to vitamin A in humans are best documented in
children born to mothers treated with the pharmaceutical Accutane, 13-cis-retinoic acid
(isotretionin) during pregnancy. Accutane entered the U.S. market in 1982 for the treatment of
severe acne, and already 3 years later Lammer et al. (1985) reported high risk for spontaneous
abortion, premature birth, perinatal mortality and major malformations associated with
exposure to the therapeutic dose. The pattern of malformations reflected the birth defects
observed in animal studies including craniofacial, cardiac, thymic, and CNS deformities. The
most frequently occurring category was CNS malformations (Lammer et al., 1985; 1988).
Furthermore, longitudinal follow-up of the children, both with and without major
malformations, indicated that 47% of the children had mental ability scores in the borderline
to the mentally retarded range (Adams and Lammer, 1993).
As opposed to oral intake, more than 25 years of topical use of RA for acne are without
evidence for increased teratogenicity. In a case control study of 215 mothers exposed to
tretinoin during pregnancy, the prevalence of major foetal malformations was 1.9 in the
treatment group versus 2.6 in the control group (Jick et al., 1993 cited in Mukherjee et al.,
2006). However, it is still being warned against using the drug retinoic acid during pregnancy.
Dermal absorption:
In vitro
Freshly biopsied human skin from abdominal surgery of 2 volunteers was used to test dermal permeation with either a gel or oil-in-water emulsion of 0.3% [3H]-retinol. The retinol dose (2 mg/cm² application amount) was applied to each diffusion cell for 24 h, and then washed off to remove any unabsorbed material. A fraction collector was used to collect receptor fluid as 6-h fractions for a total of 24 or 72 h. At the end of the study (24 or 72 h), the skin was removed from the diffusion cell and the amount of retinol remaining in the skin was determined.
Only small amounts remained in the viable skin (epidermis/dermis) or receptor fluid. The portion penetrated into the skin of human (SC, viable skin) amounted to 5.7% or 8.9% after 24 hours with values of 3.8% and 7.8% after 72 hours for the gel or emulsion, respectively.
The bioavailable portion amounted to 2.4% or 4.3% after 24 hours with values of 1.5% and 5.1% after 72 hours of the applied dose level for the gel or emulsion, respectively under the study conditions.
Freshly biopsied human skin from abdominal surgery of 3 female volunteers was placed on static diffusion cells to test dermal bioavailablity of retinyl palmitate emulsion with a content of 0.15% [14C]-retinyl palmitate ([14C]-RP) when applied for 16h. Majority the test substance was attached to the SC. Only small amounts could be detected in the remaining skin tissues and only negligible amounts in the receptor fluid. The portion penetrated into the skin (SC, epidermis, dermis) was in the range of 0.30-0.33 μg/cm² or 9.1–10.5% with respect to the applied dose. The bioavailable portion ranged between 0.033–0.036 μg/cm² corresponding to 1.1–1.24% of the applied dose level under the study conditions.
In vivo
Two groups of female volunteers were treated topically for 21 days with creams containing 0.3% retinol or 0.55% retinyl palmitate on about 3000 cm2 of their body surface (back, upper legs). Daily, 3.5 g of cream was applied comprising 9 mg of retinol or 16 mg of retinyl palmitate. Plasma levels of retinol, retinyl palmitate, retinyl oleate, retinyl stearate, 9-cis-, 13-cis-, all-trans-, 13-cis-4-oxo- or all-trans-oxo-retinoic acids were measured 0, 1, 2, 4, 6, 8, 12, 14-16 and 24 hours after each application. On day 21, no changes in plasma retinoid levels were observed.

Categories
Toxicology

E. pathways of elimination for dpm

Learning Goal: I’m working on a toxicology question and need an explanation and answer to help me learn.
Discuss the toxicology of DPM as per the following headings:
a. absorption,
b. distribution in the body and target organs,
c. pathways for biotransformation,
d. mechanisms of harm (interaction with cells and tissues)
e. pathways of elimination for DPM