The climate
is changing at a rate never seen before. Aquatic organisms are endangered
throughout the world for various reasons, including global climate change.
Changes in precipitation and temperature will dramatically affect the survival
of many species. Plants play a key role in moderating climate change becausethey take up carbon dioxide (CO2). If plants are lost, the carbon (as CO2) will
continue accumulating in our atmosphere and causes air temperature to rise,
leading to ocean acidification. With climate changes, aquatic environments face
increases in oceans salinity and sea level rise due to melting of the ice in
the poles. These combined factors result in drastic world destruction.
Organisms need specific conditions in order to survive. Scientists predict that
these conditions will be altered when the global climate changes. A change insalinity and temperature could lead to death, migration, or poor health of the
living organisms. The loss of aquatic environments will be a major disasterthat will take place because of previous changes
A general scheme is set for the estimation of the
impurities in bulk drug substances by the rational use of chromatographic,
spectroscopic and analytical techniques. The various parameters to be fulfilled
in an impurity profiling of drug substances are discussed. Impurity is definedas any substance coexisting with the original drug, such as starting materialor intermediates or these formed, due to any side reactions. The presence of
these unwanted chemicals, even in small amounts, may influence the efficacy and
safety of the pharmaceutical products. Impurity profiling (i.e., the identity
as well as the quantity of impurity in the pharmaceuticals), is now gaining
critical attention from regulatory authorities.
The different Pharmacopoeias,
such as the British Pharmacopoeia (BP), United States Pharmacopeia (USP), and
Indian Pharmacopoeia (IP) are slowly incorporating limits for allowable levels
of impurities present in the APIs or formulations. The process-relatedimpurities in an active pharmaceutical ingredient (API) can have a significantimpact on the quality and safety of the drug products. The impurity levels in
any drug substance are described as per its biological or toxicological data. It
is quite important for “regulatory” aspect of drug approval to provide
limitation of “related impurities.” Therefore, it is necessary to study the
impurity profile of any API and control it during the manufacturing of a drug
product.
Benzamide is a carbonic acid amide of benzoic
acid. Amide is a group of organic chemicals with the general formula RCO-NH2 in
which a carbon atom is attached to oxygen in double bond and also attached to
an hydroxyl group, where ‘R’ groups range from hydrogen to various linear and
ring structures or a compound with a metal replacing hydrogen in ammonia such
as sodium amide, NaNH2- Amides are divided into subclasses according to the
number of substituents on nitrogen. The primary amide is formed by replacementof the carboxylic hydroxyl group by the NH2, amino group. An example is
acetamide (acetic acid+amide). Amide is obtained by reaction of an acid
chloride, acid anhydride, or ester with an amine.
Amides are named with adding
‘-ic acid’ or ‘-oic acid’ from the name of the parent carboxylic acid and
replacing it with the suffix ‘amide’. Amide can be formed from ammonia (NH3).
The secondary and tertiary amides are the compounds in which one or bothhydrogens in primacy amides are replaced by other groups. The names of
secondary and tertiary amides are denoted by the replaced groups with the
prefix capital N (meaning nitrogen) prior to the names of parent amides. Low
molecular weight amides are soluble in water due to the formation of hydrogen
bonds. Primary amides have higher melting and boiling points than secondary and
tertiary amides.
Mitochondria generate cellular energy in the form of
adenosine triphosphate (ATP) by the process of oxidative phosphorylation. The
organelle contains a small genome that, in animals, encodes 13 essential
subunits of the respiratory chain complexes as well as all the rRNAs and tRNAs
necessary for their translation. The mitochondrial genome is more vulnerable tooxidative damage
and undergoes a higher rate of mutation than the nucleargenome. Otto
Warburg observed that tumor slices have elevated levels of glucose consumption
and lactate production in the presence of ample oxygen (termed the Warburg
effect). He later postulated that cancer originates from irreversible injury to
respiration followed by an increase in glycolysis to replace ATP loss due to
defective oxidative phosphorylation.
According to Warburg, this metabolic shift from oxidative
phosphorylation to glycolysis converts differentiated cells into
undifferentiated cells that proliferate as cancer cells. Although the
observation that tumor cells exhibit high levels of aerobic glycolysis has been
corroborated, the role of mitochondria in tumor cells has been contentious.
While multiple investigators have demonstrated that mitochondria are indeed
functional in most tumor cells, some argue that decreases in mitochondrialmetabolism and
respiratory rate are essential for tumor cell proliferation. However, the
only tumor cells shown to exhibit mitochondrial dysfunction are those that have
mutations in the tricarboxylic acid cycle enzymes succinate dehydrogenase or
fumarate hydratase. Furthermore, oncogene activation increases mitochondrial
metabolism, correlating with metastatic potential.
