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Ventilatory parameters such as tidal volume, minute ventilation (V_E), and inspiratory flow rate decrease in 24- vs. 12-month-old male and female rats. Differences between male and female values are maintained with age. Ventilatory response male and female rats exhibit to hypercapnia is altered by a decrease of the intercept, but not the slope value. The pattern of breathing exhibited by young females and males in response to hypercapnia (i.e. an increase of V_T and f) is different than that noted in old males and females (i.e. an increase in V_T only). In contrast, the ventilatory response both of slope and intercept male rats show by 24 months is decreased compared to the 12-month value; but the slope value is actually increased in the older vs. younger female rats in response to hypoxia.

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This review examines and evaluates the literature on the ability of inorganic arsenic compounds to cause cancer in humans and laboratory animals. The epidemiological data that supports the position that inorganic arsenical derivatives are carcinogenic in humans is convincing and difficult to deny because of their consistency. These data are from studies of different occupational exposures such as smelter and pesticide workers, as well as from studies of drinking water, wines and medicinal tonics that contained or were contaminated with inorganic compounds of arsenic. Indeed, positive dose-response relationships between cancer incidence or mortality with many inorganic arsenical substances have been shown. Despite the presence of data which confuse the interpretation and evaluation of epidemiological data, associated neoplasms of the lungs, skin and gastrointestinal systems have been observed as a result of exposure to inorganic arsenic compounds.The mechanism of carcinogenicity of inorganic arsenical substances in humans is unknown. Inorganic arsenic compounds are not carcinogenic in laboratory animals by most routes of administration. However, further studies (subchronic, chronic, carcinogenic) using intratracheal and other conventional routes in other animal species would appear to be warranted. Moreso, especially since there is no evidence that organic arsenic compounds are carcinogenic in numerous mammalian species. Inorganic derivatives of arsenic are not mutagenic but may be teraiogenic. This latter conclusion is dependent on the method of administration and size of the dose, as well as on the species of animal used for the study.

In this study ventilation was evaluated in 12-mo-old male and female rats who had received large doses of aspartic acid neonatally. Rats of both sexes treated with aspartic acid were obese, stunted, and exhibited hypogonadism. Although metabolic rates of the aspartic acid-treated rats were not different compared with sex-matched controls, ventilatory patterns were different. Aspartic acid-treated females breathed with a smaller tidal volume (VT), higher frequency (f), and similar minute ventilation (VE) compared with control females. This pattern is commonly observed in many patients who are obese. The aspartic acid-treated females responded to hypercapnic and hypoxic challenges by increasing f more than VT. Tissue pocket gases (PCO2 and PO2) of aspartic acid-treated females were normal. In contrast, aspartic acid-treated males hypoventilated compared with control males. Tissue pocket gas values suggested that aspartic acid-treated males were hypoxemic and hypercapnic. Moreover, the response of aspartic acid-treated males to hypercapnia was parallel to but was less than that of control male rats. The ventilatory response of aspartic acid-treated male rats to hypoxia was blunted. This study has shown that neonatal administration of aspartic acid causes a decreased ventilation and blunted response to hypoxia in adult male but not female rats.

Previously we observed that acute subcutaneous administration of aspartic acid (580 mg/kg) depressed ventilation in awake male, but not female, rats, suggesting that this agent may be used as a marker for sexual dimorphism in the control of ventilation. Moreover, males castrated postpubertally showed a response similar to that of intact male rats. Thus the hormonal milieu of male rats appear not to be necessary to elicit the masculine type of ventilatory response to aspartic acid. The purpose of this study was 1) to determine whether adult female rats androgenized by the administration of testosterone propionate (TP) 1 day after birth would alter their ventilation in response to aspartic acid to be more malelike and 2) to compare these results with those of intact (I) and ovariectomized (O) female rats. Minute ventilation and O2 consumption in air and in response to aspartic acid administration were evaluated in awake animals in all three groups. Furthermore the minute ventilation of all rats to a hypercapnic challenge was also evaluated. Ovariectomy resulted in rats increased body weights but decreased weight-corrected ventilation and O2 consumption compared with TP-treated and I animals. Minute ventilation after hypercapnic challenge in the three groups was similar. TP-treated rats responded to aspartic acid administration with a marked depression of ventilation similar to that previously noted in males, whereas neither I nor O rats showed such a response. The depression of ventilation in the TP-treated group in response to aspartic acid was not a consequence of a depression of O2 consumption.(ABSTRACT TRUNCATED AT 250 WORDS)

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