Answer:
Hepato- and nephrotoxicity of fluoride have been demonstrated in animals, but few studies have examined potential effects in humans. This population-based study examines the relationship between chronic low-level fluoride exposure and kidney and liver function among United States (U.S.) adolescents. This study aimed to evaluate whether greater fluoride exposure is associated with altered kidney and liver parameters among U.S. youth.
This cross-sectional study utilized data from the National Health and Nutrition Examination Survey (2013–2016). We analyzed data from 1983 and 1742 adolescents who had plasma and water fluoride measures respectively and did not have kidney disease. Fluoride was measured in plasma and household tap water. Kidney parameters included estimated glomerular filtration rate (calculated by the original Schwartz formula), serum uric acid, and the urinary albumin to creatinine ratio. Liver parameters were assessed in serum and included alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, blood urea nitrogen, gamma-glutamyl transferase, and albumin. Survey-weighted linear regression examined relationships between fluoride exposure and kidney and liver parameters after covariate adjustment. A Holm-Bonferroni correction accounted for multiple comparisons.
The average age of adolescents was 15.4 years. Median water and plasma fluoride concentrations were 0.48 mg/L and 0.33 μmol/L respectively. A 1 μmol/L increase in plasma fluoride was associated with a 10.36 mL/min/1.73 m2 lower estimated glomerular filtration rate (95% CI: −17.50, −3.22; p = 0.05), a 0.29 mg/dL higher serum uric acid concentration (95% CI: 0.09, 0.50; p = 0.05), and a 1.29 mg/dL lower blood urea nitrogen concentration (95%CI: −1.87, −0.70; p < 0.001). A 1 mg/L increase in water fluoride was associated with a 0.93 mg/dL lower blood urea nitrogen concentration (95% CI: −1.44, −0.42; p = 0.007).
Fluoride exposure may contribute to complex changes in kidney and liver related parameters among U.S. adolescents. As the study is cross-sectional, reverse causality cannot be ruled out; therefore, altered kidney and/or liver function may impact bodily fluoride absorption and metabolic processes.
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This would be an example of:
C) an insertion mutation.
Notice how the sequence contains the same letters as before, only an A is added to the beginning. Adding extra nucleotides is an example of an insertion mutation, a type of frame-shift also, because the reading frame will be thrown off downstream.
Answer:
Renin; angiotensin I and angiotensin II
Explanation:
Renin is a key hormone involved in the renin-angiotensin-aldosterone system (RAAS), which is responsible for regulating blood pressure in response to changes in blood volume. Renin is secreted primarily by the kidneys to promote the production of the peptide hormone angiotensin in the blood vessels. Subsequently, angiotensin stimulates the release of aldosterone from the adrenal cortex, stimulating sodium retention by the kidneys. Renin acts on its substrate angiotensinogen to yield angiotensin I, which is then converted to angiotensin II by the angiotensin-converting enzyme (ACE). Finally, angiotensin 2 promotes the release of aldosterone by the adrenal cortex, which acts on renal tubules, leading to the reabsorption of sodium and water and the excretion of potassium.
